Voltage-dependent cell membrane glycoproteins selectively permeable to calcium ions. They are categorized as L-, T-, N-, P-, Q-, and R-types based on the activation and inactivation kinetics, ion specificity, and sensitivity to drugs and toxins. The L- and T-types are present throughout the cardiovascular and central nervous systems and the N-, P-, Q-, & R-types are located in neuronal tissue.
A class of drugs that act by selective inhibition of calcium influx through cellular membranes.
Long-lasting voltage-gated CALCIUM CHANNELS found in both excitable and nonexcitable tissue. They are responsible for normal myocardial and vascular smooth muscle contractility. Five subunits (alpha-1, alpha-2, beta, gamma, and delta) make up the L-type channel. The alpha-1 subunit is the binding site for calcium-based antagonists. Dihydropyridine-based calcium antagonists are used as markers for these binding sites.
Gated, ion-selective glycoproteins that traverse membranes. The stimulus for ION CHANNEL GATING can be due to a variety of stimuli such as LIGANDS, a TRANSMEMBRANE POTENTIAL DIFFERENCE, mechanical deformation or through INTRACELLULAR SIGNALING PEPTIDES AND PROTEINS.
CALCIUM CHANNELS that are concentrated in neural tissue. Omega toxins inhibit the actions of these channels by altering their voltage dependence.
A heterogenous group of transient or low voltage activated type CALCIUM CHANNELS. They are found in cardiac myocyte membranes, the sinoatrial node, Purkinje cells of the heart and the central nervous system.
Signal transduction mechanisms whereby calcium mobilization (from outside the cell or from intracellular storage pools) to the cytoplasm is triggered by external stimuli. Calcium signals are often seen to propagate as waves, oscillations, spikes, sparks, or puffs. The calcium acts as an intracellular messenger by activating calcium-responsive proteins.
Agents that increase calcium influx into calcium channels of excitable tissues. This causes vasoconstriction in VASCULAR SMOOTH MUSCLE and/or CARDIAC MUSCLE cells as well as stimulation of insulin release from pancreatic islets. Therefore, tissue-selective calcium agonists have the potential to combat cardiac failure and endocrinological disorders. They have been used primarily in experimental studies in cell and tissue culture.
The opening and closing of ion channels due to a stimulus. The stimulus can be a change in membrane potential (voltage-gated), drugs or chemical transmitters (ligand-gated), or a mechanical deformation. Gating is thought to involve conformational changes of the ion channel which alters selective permeability.
Potassium channels where the flow of K+ ions into the cell is greater than the outward flow.
CALCIUM CHANNELS located within the PURKINJE CELLS of the cerebellum. They are involved in stimulation-secretion coupling of neurons.
CALCIUM CHANNELS located in the neurons of the brain.
Pyridine moieties which are partially saturated by the addition of two hydrogen atoms in any position.
CALCIUM CHANNELS located in the neurons of the brain. They are inhibited by the marine snail toxin, omega conotoxin MVIIC.
A potent vasodilator agent with calcium antagonistic action. It is a useful anti-anginal agent that also lowers blood pressure.
A class of drugs that act by inhibition of potassium efflux through cell membranes. Blockade of potassium channels prolongs the duration of ACTION POTENTIALS. They are used as ANTI-ARRHYTHMIA AGENTS and VASODILATOR AGENTS.
Cell membrane glycoproteins that form channels to selectively pass chloride ions. Nonselective blockers include FENAMATES; ETHACRYNIC ACID; and TAMOXIFEN.
A neurotoxic peptide, which is a cleavage product (VIa) of the omega-Conotoxin precursor protein contained in venom from the marine snail, CONUS geographus. It is an antagonist of CALCIUM CHANNELS, N-TYPE.
The study of the generation and behavior of electrical charges in living organisms particularly the nervous system and the effects of electricity on living organisms.
Calcium compounds used as food supplements or in food to supply the body with calcium. Dietary calcium is needed during growth for bone development and for maintenance of skeletal integrity later in life to prevent osteoporosis.
The voltage differences across a membrane. For cellular membranes they are computed by subtracting the voltage measured outside the membrane from the voltage measured inside the membrane. They result from differences of inside versus outside concentration of potassium, sodium, chloride, and other ions across cells' or ORGANELLES membranes. For excitable cells, the resting membrane potentials range between -30 and -100 millivolts. Physical, chemical, or electrical stimuli can make a membrane potential more negative (hyperpolarization), or less negative (depolarization).
A family of structurally related neurotoxic peptides from mollusk venom that inhibit voltage-activated entry of calcium into the presynaptic membrane. They selectively inhibit N-, P-, and Q-type calcium channels.
Potassium channel whose permeability to ions is extremely sensitive to the transmembrane potential difference. The opening of these channels is induced by the membrane depolarization of the ACTION POTENTIAL.
A benzothiazepine derivative with vasodilating action due to its antagonism of the actions of CALCIUM ion on membrane functions.
Heteromultimers of Kir6 channels (the pore portion) and sulfonylurea receptor (the regulatory portion) which affect function of the HEART; PANCREATIC BETA CELLS; and KIDNEY COLLECTING DUCTS. KATP channel blockers include GLIBENCLAMIDE and mitiglinide whereas openers include CROMAKALIM and minoxidil sulfate.
A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes.
A calcium channel blocker that is a class IV anti-arrhythmia agent.
A potent antagonist of CALCIUM CHANNELS that is highly selective for VASCULAR SMOOTH MUSCLE. It is effective in the treatment of chronic stable angina pectoris, hypertension, and congestive cardiac failure.
An electrophysiologic technique for studying cells, cell membranes, and occasionally isolated organelles. All patch-clamp methods rely on a very high-resistance seal between a micropipette and a membrane; the seal is usually attained by gentle suction. The four most common variants include on-cell patch, inside-out patch, outside-out patch, and whole-cell clamp. Patch-clamp methods are commonly used to voltage clamp, that is control the voltage across the membrane and measure current flow, but current-clamp methods, in which the current is controlled and the voltage is measured, are also used.
Potassium channels whose activation is dependent on intracellular calcium concentrations.
A calcium channel blocker with marked vasodilator action. It is an effective antihypertensive agent and differs from other calcium channel blockers in that it does not reduce glomerular filtration rate and is mildly natriuretic, rather than sodium retentive.
A benzimidazoyl-substituted tetraline that selectively binds and inhibits CALCIUM CHANNELS, T-TYPE.
The ability of a substrate to allow the passage of ELECTRONS.
A class of drugs that act by inhibition of sodium influx through cell membranes. Blockade of sodium channels slows the rate and amplitude of initial rapid depolarization, reduces cell excitability, and reduces conduction velocity.
An element of the alkaline earth group of metals. It has an atomic symbol Ba, atomic number 56, and atomic weight 138. All of its acid-soluble salts are poisonous.
A calcium channel blockader with preferential cerebrovascular activity. It has marked cerebrovascular dilating effects and lowers blood pressure.
A neuropeptide toxin from the venom of the funnel web spider, Agelenopsis aperta. It inhibits CALCIUM CHANNELS, P-TYPE by altering the voltage-dependent gating so that very large depolarizations are needed for channel opening. It also inhibits CALCIUM CHANNELS, Q-TYPE.
A subgroup of TRP cation channels that contain 3-4 ANKYRIN REPEAT DOMAINS and a conserved C-terminal domain. Members are highly expressed in the CENTRAL NERVOUS SYSTEM. Selectivity for calcium over sodium ranges from 0.5 to 10.
Voltage-gated potassium channels whose primary subunits contain six transmembrane segments and form tetramers to create a pore with a voltage sensor. They are related to their founding member, shaker protein, Drosophila.
The rate dynamics in chemical or physical systems.
The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the NERVOUS SYSTEM.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
A major class of calcium activated potassium channels whose members are voltage-dependent. MaxiK channels are activated by either membrane depolarization or an increase in intracellular Ca(2+). They are key regulators of calcium and electrical signaling in a variety of tissues.
An element in the alkali group of metals with an atomic symbol K, atomic number 19, and atomic weight 39.10. It is the chief cation in the intracellular fluid of muscle and other cells. Potassium ion is a strong electrolyte that plays a significant role in the regulation of fluid volume and maintenance of the WATER-ELECTROLYTE BALANCE.
Carbonic acid calcium salt (CaCO3). An odorless, tasteless powder or crystal that occurs in nature. It is used therapeutically as a phosphate buffer in hemodialysis patients and as a calcium supplement.
A subgroup of cyclic nucleotide-regulated ION CHANNELS within the superfamily of pore-loop cation channels. They are expressed in OLFACTORY NERVE cilia and in PHOTORECEPTOR CELLS and some PLANTS.
Female germ cells derived from OOGONIA and termed OOCYTES when they enter MEIOSIS. The primary oocytes begin meiosis but are arrested at the diplotene state until OVULATION at PUBERTY to give rise to haploid secondary oocytes or ova (OVUM).
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
A salt used to replenish calcium levels, as an acid-producing diuretic, and as an antidote for magnesium poisoning.
A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.
A subgroup of TRP cation channels named after vanilloid receptor. They are very sensitive to TEMPERATURE and hot spicy food and CAPSAICIN. They have the TRP domain and ANKYRIN repeats. Selectivity for CALCIUM over SODIUM ranges from 3 to 100 fold.
The relationship between the dose of an administered drug and the response of the organism to the drug.
A potent calcium channel blockader with marked vasodilator action. It has antihypertensive properties and is effective in the treatment of angina and coronary spasms without showing cardiodepressant effects. It has also been used in the treatment of asthma and enhances the action of specific antineoplastic agents.
The commonest and widest ranging species of the clawed "frog" (Xenopus) in Africa. This species is used extensively in research. There is now a significant population in California derived from escaped laboratory animals.
The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.
A tetrameric calcium release channel in the SARCOPLASMIC RETICULUM membrane of SMOOTH MUSCLE CELLS, acting oppositely to SARCOPLASMIC RETICULUM CALCIUM-TRANSPORTING ATPASES. It is important in skeletal and cardiac excitation-contraction coupling and studied by using RYANODINE. Abnormalities are implicated in CARDIAC ARRHYTHMIAS and MUSCULAR DISEASES.
A subgroup of TRP cation channels named after melastatin protein. They have the TRP domain but lack ANKYRIN repeats. Enzyme domains in the C-terminus leads to them being called chanzymes.
A family of proton-gated sodium channels that are primarily expressed in neuronal tissue. They are AMILORIDE-sensitive and are implicated in the signaling of a variety of neurological stimuli, most notably that of pain in response to acidic conditions.
Venoms of arthropods of the order Araneida of the ARACHNIDA. The venoms usually contain several protein fractions, including ENZYMES, hemolytic, neurolytic, and other TOXINS, BIOLOGICAL.
Calcium salts of phosphoric acid. These compounds are frequently used as calcium supplements.
Established cell cultures that have the potential to propagate indefinitely.
Sodium channels found on salt-reabsorbing EPITHELIAL CELLS that line the distal NEPHRON; the distal COLON; SALIVARY DUCTS; SWEAT GLANDS; and the LUNG. They are AMILORIDE-sensitive and play a critical role in the control of sodium balance, BLOOD VOLUME, and BLOOD PRESSURE.
A delayed rectifier subtype of shaker potassium channels that is the predominant VOLTAGE-GATED POTASSIUM CHANNEL of T-LYMPHOCYTES.
A family of voltage-gated potassium channels that are characterized by long N-terminal and C-terminal intracellular tails. They are named from the Drosophila protein whose mutation causes abnormal leg shaking under ether anesthesia. Their activation kinetics are dependent on extracellular MAGNESIUM and PROTON concentration.
Stable calcium atoms that have the same atomic number as the element calcium, but differ in atomic weight. Ca-42-44, 46, and 48 are stable calcium isotopes.
A delayed rectifier subtype of shaker potassium channels that is selectively inhibited by a variety of SCORPION VENOMS.
A delayed rectifier subtype of shaker potassium channels that is commonly mutated in human episodic ATAXIA and MYOKYMIA.
Unstable isotopes of calcium that decay or disintegrate emitting radiation. Ca atoms with atomic weights 39, 41, 45, 47, 49, and 50 are radioactive calcium isotopes.
Single chains of amino acids that are the units of multimeric PROTEINS. Multimeric proteins can be composed of identical or non-identical subunits. One or more monomeric subunits may compose a protomer which itself is a subunit structure of a larger assembly.
A long-acting dihydropyridine calcium channel blocker. It is effective in the treatment of ANGINA PECTORIS and HYPERTENSION.
A delayed rectifier subtype of shaker potassium channels that conducts a delayed rectifier current. It contributes to ACTION POTENTIAL repolarization of MYOCYTES in HEART ATRIA.
A class of polyamine and peptide toxins which are isolated from the venom of spiders such as Agelenopsis aperta.
An aquatic genus of the family, Pipidae, occurring in Africa and distinguished by having black horny claws on three inner hind toes.
The muscle tissue of the HEART. It is composed of striated, involuntary muscle cells (MYOCYTES, CARDIAC) connected to form the contractile pump to generate blood flow.
A major class of calcium-activated potassium channels that are found primarily in excitable CELLS. They play important roles in the transmission of ACTION POTENTIALS and generate a long-lasting hyperpolarization known as the slow afterhyperpolarization.
A member of the alkali group of metals. It has the atomic symbol Na, atomic number 11, and atomic weight 23.
Abrupt changes in the membrane potential that sweep along the CELL MEMBRANE of excitable cells in response to excitation stimuli.
The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.
The movement of ions across energy-transducing cell membranes. Transport can be active, passive or facilitated. Ions may travel by themselves (uniport), or as a group of two or more ions in the same (symport) or opposite (antiport) directions.
Elements of limited time intervals, contributing to particular results or situations.
An adenine nucleotide containing three phosphate groups esterified to the sugar moiety. In addition to its crucial roles in metabolism adenosine triphosphate is a neurotransmitter.
Venoms from mollusks, including CONUS and OCTOPUS species. The venoms contain proteins, enzymes, choline derivatives, slow-reacting substances, and several characterized polypeptide toxins that affect the nervous system. Mollusk venoms include cephalotoxin, venerupin, maculotoxin, surugatoxin, conotoxins, and murexine.
A broad group of eukaryotic six-transmembrane cation channels that are classified by sequence homology because their functional involvement with SENSATION is varied. They have only weak voltage sensitivity and ion selectivity. They are named after a DROSOPHILA mutant that displayed transient receptor potentials in response to light. A 25-amino-acid motif containing a TRP box (EWKFAR) just C-terminal to S6 is found in TRPC, TRPV and TRPM subgroups. ANKYRIN repeats are found in TRPC, TRPV & TRPN subgroups. Some are functionally associated with TYROSINE KINASE or TYPE C PHOSPHOLIPASES.
A family of delayed rectifier voltage-gated potassium channels that share homology with their founding member, KCNQ1 PROTEIN. KCNQ potassium channels have been implicated in a variety of diseases including LONG QT SYNDROME; DEAFNESS; and EPILEPSY.
A subfamily of shaker potassium channels that shares homology with its founding member, Shab protein, Drosophila. They regulate delayed rectifier currents in the NERVOUS SYSTEM of DROSOPHILA and in the SKELETAL MUSCLE and HEART of VERTEBRATES.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
A voltage-gated potassium channel that is expressed primarily in the HEART.
A chelating agent relatively more specific for calcium and less toxic than EDETIC ACID.
Use of electric potential or currents to elicit biological responses.
The lipid- and protein-containing, selectively permeable membrane that surrounds the cytoplasm in prokaryotic and eukaryotic cells.
A shaker subfamily that is prominently expressed in NEURONS and are necessary for high-frequency, repetitive firing of ACTION POTENTIALS.
A fast inactivating subtype of shaker potassium channels that contains two inactivation domains at its N terminus.
An aminoperhydroquinazoline poison found mainly in the liver and ovaries of fishes in the order TETRAODONTIFORMES, which are eaten. The toxin causes paresthesia and paralysis through interference with neuromuscular conduction.
The level of protein structure in which combinations of secondary protein structures (alpha helices, beta sheets, loop regions, and motifs) pack together to form folded shapes called domains. Disulfide bridges between cysteines in two different parts of the polypeptide chain along with other interactions between the chains play a role in the formation and stabilization of tertiary structure. Small proteins usually consist of only one domain but larger proteins may contain a number of domains connected by segments of polypeptide chain which lack regular secondary structure.
Theoretical representations that simulate the behavior or activity of biological processes or diseases. For disease models in living animals, DISEASE MODELS, ANIMAL is available. Biological models include the use of mathematical equations, computers, and other electronic equipment.
The calcium salt of oxalic acid, occurring in the urine as crystals and in certain calculi.
Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.
Chemicals that bind to and remove ions from solutions. Many chelating agents function through the formation of COORDINATION COMPLEXES with METALS.
Coronary vasodilator that is an analog of iproveratril (VERAPAMIL) with one more methoxy group on the benzene ring.
A family of inwardly-rectifying potassium channels that are activated by PERTUSSIS TOXIN sensitive G-PROTEIN-COUPLED RECEPTORS. GIRK potassium channels are primarily activated by the complex of GTP-BINDING PROTEIN BETA SUBUNITS and GTP-BINDING PROTEIN GAMMA SUBUNITS.
The calcium salt of gluconic acid. The compound has a variety of uses, including its use as a calcium replenisher in hypocalcemic states.
A shaker subfamily of potassium channels that participate in transient outward potassium currents by activating at subthreshold MEMBRANE POTENTIALS, inactivating rapidly, and recovering from inactivation quickly.
The distal terminations of axons which are specialized for the release of neurotransmitters. Also included are varicosities along the course of axons which have similar specializations and also release transmitters. Presynaptic terminals in both the central and peripheral nervous systems are included.
A metallic element that has the atomic symbol Mg, atomic number 12, and atomic weight 24.31. It is important for the activity of many enzymes, especially those involved in OXIDATIVE PHOSPHORYLATION.
A fluorescent calcium chelating agent which is used to study intracellular calcium in tissues.
Members of the class of compounds composed of AMINO ACIDS joined together by peptide bonds between adjacent amino acids into linear, branched or cyclical structures. OLIGOPEPTIDES are composed of approximately 2-12 amino acids. Polypeptides are composed of approximately 13 or more amino acids. PROTEINS are linear polypeptides that are normally synthesized on RIBOSOMES.
A sesquiterpene lactone found in roots of THAPSIA. It inhibits CA(2+)-TRANSPORTING ATPASE mediated uptake of CALCIUM into SARCOPLASMIC RETICULUM.
The hollow, muscular organ that maintains the circulation of the blood.
A very slow opening and closing voltage-gated potassium channel that is expressed in NEURONS and is commonly mutated in BENIGN FAMILIAL NEONATAL CONVULSIONS.
The parts of a macromolecule that directly participate in its specific combination with another molecule.
A subgroup of cyclic nucleotide-regulated ION CHANNELS of the superfamily of pore-loop cation channels that are opened by hyperpolarization rather than depolarization. The ion conducting pore passes SODIUM, CALCIUM, and POTASSIUM cations with a preference for potassium.
The uptake of naked or purified DNA by CELLS, usually meaning the process as it occurs in eukaryotic cells. It is analogous to bacterial transformation (TRANSFORMATION, BACTERIAL) and both are routinely employed in GENE TRANSFER TECHNIQUES.
A common name used for the genus Cavia. The most common species is Cavia porcellus which is the domesticated guinea pig used for pets and biomedical research.
The nonstriated involuntary muscle tissue of blood vessels.
A potassium-selective ion channel blocker. (From J Gen Phys 1994;104(1):173-90)
A trace element with the atomic symbol Ni, atomic number 28, and atomic weight 58.69. It is a cofactor of the enzyme UREASE.
Substances used for their pharmacological actions on any aspect of neurotransmitter systems. Neurotransmitter agents include agonists, antagonists, degradation inhibitors, uptake inhibitors, depleters, precursors, and modulators of receptor function.
The study of PHYSICAL PHENOMENA and PHYSICAL PROCESSES as applied to living things.
An antidiabetic sulfonylurea derivative with actions similar to those of chlorpropamide.
The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.
Lanthanum. The prototypical element in the rare earth family of metals. It has the atomic symbol La, atomic number 57, and atomic weight 138.91. Lanthanide ion is used in experimental biology as a calcium antagonist; lanthanum oxide improves the optical properties of glass.
An element with atomic symbol Cd, atomic number 48, and atomic weight 114. It is a metal and ingestion will lead to CADMIUM POISONING.
Venoms from animals of the order Scorpionida of the class Arachnida. They contain neuro- and hemotoxins, enzymes, and various other factors that may release acetylcholine and catecholamines from nerve endings. Of the several protein toxins that have been characterized, most are immunogenic.
Contractile tissue that produces movement in animals.
A dihydropyridine calcium channel antagonist that acts as a potent arterial vasodilator and antihypertensive agent. It is also effective in patients with cardiac failure and angina.
A voltage-gated sodium channel subtype that mediates the sodium ion PERMEABILITY of CARDIOMYOCYTES. Defects in the SCN5A gene, which codes for the alpha subunit of this sodium channel, are associated with a variety of CARDIAC DISEASES that result from loss of sodium channel function.
A curved elevation of GRAY MATTER extending the entire length of the floor of the TEMPORAL HORN of the LATERAL VENTRICLE (see also TEMPORAL LOBE). The hippocampus proper, subiculum, and DENTATE GYRUS constitute the hippocampal formation. Sometimes authors include the ENTORHINAL CORTEX in the hippocampal formation.
Models used experimentally or theoretically to study molecular shape, electronic properties, or interactions; includes analogous molecules, computer-generated graphics, and mechanical structures.
A major class of calcium-activated potassium channels that were originally discovered in ERYTHROCYTES. They are found primarily in non-excitable CELLS and set up electrical gradients for PASSIVE ION TRANSPORT.
Proteins which are found in membranes including cellular and intracellular membranes. They consist of two types, peripheral and integral proteins. They include most membrane-associated enzymes, antigenic proteins, transport proteins, and drug, hormone, and lectin receptors.
The communication from a NEURON to a target (neuron, muscle, or secretory cell) across a SYNAPSE. In chemical synaptic transmission, the presynaptic neuron releases a NEUROTRANSMITTER that diffuses across the synaptic cleft and binds to specific synaptic receptors, activating them. The activated receptors modulate specific ion channels and/or second-messenger systems in the postsynaptic cell. In electrical synaptic transmission, electrical signals are communicated as an ionic current flow across ELECTRICAL SYNAPSES.
A very slow opening and closing voltage-gated potassium channel that is expressed in NEURONS and is closely related to KCNQ2 POTASSIUM CHANNEL. It is commonly mutated in BENIGN FAMILIAL NEONATAL CONVULSIONS.
The pore-forming subunits of large-conductance calcium-activated potassium channels. They form tetramers in CELL MEMBRANES.
An atom or group of atoms that have a positive or negative electric charge due to a gain (negative charge) or loss (positive charge) of one or more electrons. Atoms with a positive charge are known as CATIONS; those with a negative charge are ANIONS.
Sensory ganglia located on the dorsal spinal roots within the vertebral column. The spinal ganglion cells are pseudounipolar. The single primary branch bifurcates sending a peripheral process to carry sensory information from the periphery and a central branch which relays that information to the spinal cord or brain.
The normality of a solution with respect to HYDROGEN ions; H+. It is related to acidity measurements in most cases by pH = log 1/2[1/(H+)], where (H+) is the hydrogen ion concentration in gram equivalents per liter of solution. (McGraw-Hill Dictionary of Scientific and Technical Terms, 6th ed)
Positively charged atoms, radicals or groups of atoms which travel to the cathode or negative pole during electrolysis.
Intracellular receptors that bind to INOSITOL 1,4,5-TRISPHOSPHATE and play an important role in its intracellular signaling. Inositol 1,4,5-trisphosphate receptors are calcium channels that release CALCIUM in response to increased levels of inositol 1,4,5-trisphosphate in the CYTOPLASM.
The process in which substances, either endogenous or exogenous, bind to proteins, peptides, enzymes, protein precursors, or allied compounds. Specific protein-binding measures are often used as assays in diagnostic assessments.
A process leading to shortening and/or development of tension in muscle tissue. Muscle contraction occurs by a sliding filament mechanism whereby actin filaments slide inward among the myosin filaments.
A methylpyrrole-carboxylate from RYANIA that disrupts the RYANODINE RECEPTOR CALCIUM RELEASE CHANNEL to modify CALCIUM release from SARCOPLASMIC RETICULUM resulting in alteration of MUSCLE CONTRACTION. It was previously used in INSECTICIDES. It is used experimentally in conjunction with THAPSIGARGIN and other inhibitors of CALCIUM ATPASE uptake of calcium into SARCOPLASMIC RETICULUM.
A group of slow opening and closing voltage-gated potassium channels. Because of their delayed activation kinetics they play an important role in controlling ACTION POTENTIAL duration.
A heat-stable, low-molecular-weight activator protein found mainly in the brain and heart. The binding of calcium ions to this protein allows this protein to bind to cyclic nucleotide phosphodiesterases and to adenyl cyclase with subsequent activation. Thereby this protein modulates cyclic AMP and cyclic GMP levels.
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
A voltage-gated sodium channel subtype that mediates the sodium ion permeability of excitable membranes. Defects in the SCN2A gene which codes for the alpha subunit of this sodium channel are associated with benign familial infantile seizures type 3, and early infantile epileptic encephalopathy type 11.
A family of membrane proteins that selectively conduct SODIUM ions due to changes in the TRANSMEMBRANE POTENTIAL DIFFERENCE. They typically have a multimeric structure with a core alpha subunit that defines the sodium channel subtype and several beta subunits that modulate sodium channel activity.
Inorganic compounds derived from hydrochloric acid that contain the Cl- ion.
Striated muscle cells found in the heart. They are derived from cardiac myoblasts (MYOBLASTS, CARDIAC).
A quality of cell membranes which permits the passage of solvents and solutes into and out of cells.
A 37-amino acid residue peptide isolated from the scorpion Leiurus quinquestriatus hebraeus. It is a neurotoxin that inhibits calcium activated potassium channels.
Layers of lipid molecules which are two molecules thick. Bilayer systems are frequently studied as models of biological membranes.
The physical characteristics and processes of biological systems.
Proteins prepared by recombinant DNA technology.
The fluid inside CELLS.
Refers to animals in the period of time just after birth.
Intracellular fluid from the cytoplasm after removal of ORGANELLES and other insoluble cytoplasmic components.
An element of the alkaline earth family of metals. It has the atomic symbol Sr, atomic number 38, and atomic weight 87.62.
Flunarizine is a selective calcium entry blocker with calmodulin binding properties and histamine H1 blocking activity. It is effective in the prophylaxis of migraine, occlusive peripheral vascular disease, vertigo of central and peripheral origin, and as an adjuvant in the therapy of epilepsy.
An ionophorous, polyether antibiotic from Streptomyces chartreusensis. It binds and transports CALCIUM and other divalent cations across membranes and uncouples oxidative phosphorylation while inhibiting ATPase of rat liver mitochondria. The substance is used mostly as a biochemical tool to study the role of divalent cations in various biological systems.
A cell line generated from human embryonic kidney cells that were transformed with human adenovirus type 5.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
Regulatory proteins that act as molecular switches. They control a wide range of biological processes including: receptor signaling, intracellular signal transduction pathways, and protein synthesis. Their activity is regulated by factors that control their ability to bind to and hydrolyze GTP to GDP. EC 3.6.1.-.
The characteristic 3-dimensional shape of a protein, including the secondary, supersecondary (motifs), tertiary (domains) and quaternary structure of the peptide chain. PROTEIN STRUCTURE, QUATERNARY describes the conformation assumed by multimeric proteins (aggregates of more than one polypeptide chain).
Agents that emit light after excitation by light. The wave length of the emitted light is usually longer than that of the incident light. Fluorochromes are substances that cause fluorescence in other substances, i.e., dyes used to mark or label other compounds with fluorescent tags.
Inorganic compounds that contain calcium as an integral part of the molecule.
Different forms of a protein that may be produced from different GENES, or from the same gene by ALTERNATIVE SPLICING.
A non-essential amino acid naturally occurring in the L-form. Glutamic acid is the most common excitatory neurotransmitter in the CENTRAL NERVOUS SYSTEM.
One of the POTASSIUM CHANNEL BLOCKERS, with secondary effect on calcium currents, which is used mainly as a research tool and to characterize channel subtypes.
Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.
An adenine nucleotide containing one phosphate group which is esterified to both the 3'- and 5'-positions of the sugar moiety. It is a second messenger and a key intracellular regulator, functioning as a mediator of activity for a number of hormones, including epinephrine, glucagon, and ACTH.
Specialized junctions at which a neuron communicates with a target cell. At classical synapses, a neuron's presynaptic terminal releases a chemical transmitter stored in synaptic vesicles which diffuses across a narrow synaptic cleft and activates receptors on the postsynaptic membrane of the target cell. The target may be a dendrite, cell body, or axon of another neuron, or a specialized region of a muscle or secretory cell. Neurons may also communicate via direct electrical coupling with ELECTRICAL SYNAPSES. Several other non-synaptic chemical or electric signal transmitting processes occur via extracellular mediated interactions.
Positively charged atoms, radicals or groups of atoms with a valence of plus 2, which travel to the cathode or negative pole during electrolysis.
A highly neurotoxic polypeptide from the venom of the honey bee (Apis mellifera). It consists of 18 amino acids with two disulfide bridges and causes hyperexcitability resulting in convulsions and respiratory paralysis.
An serine-threonine protein kinase that requires the presence of physiological concentrations of CALCIUM and membrane PHOSPHOLIPIDS. The additional presence of DIACYLGLYCEROLS markedly increases its sensitivity to both calcium and phospholipids. The sensitivity of the enzyme can also be increased by PHORBOL ESTERS and it is believed that protein kinase C is the receptor protein of tumor-promoting phorbol esters.
The relationship between the chemical structure of a compound and its biological or pharmacological activity. Compounds are often classed together because they have structural characteristics in common including shape, size, stereochemical arrangement, and distribution of functional groups.
A group of enzymes that are dependent on CYCLIC AMP and catalyze the phosphorylation of SERINE or THREONINE residues on proteins. Included under this category are two cyclic-AMP-dependent protein kinase subtypes, each of which is defined by its subunit composition.
Proteins to which calcium ions are bound. They can act as transport proteins, regulator proteins, or activator proteins. They typically contain EF HAND MOTIFS.
A white crystal or crystalline powder used in BUFFERS; FERTILIZERS; and EXPLOSIVES. It can be used to replenish ELECTROLYTES and restore WATER-ELECTROLYTE BALANCE in treating HYPOKALEMIA.
A methylxanthine naturally occurring in some beverages and also used as a pharmacological agent. Caffeine's most notable pharmacological effect is as a central nervous system stimulant, increasing alertness and producing agitation. It also relaxes SMOOTH MUSCLE, stimulates CARDIAC MUSCLE, stimulates DIURESIS, and appears to be useful in the treatment of some types of headache. Several cellular actions of caffeine have been observed, but it is not entirely clear how each contributes to its pharmacological profile. Among the most important are inhibition of cyclic nucleotide PHOSPHODIESTERASES, antagonism of ADENOSINE RECEPTORS, and modulation of intracellular calcium handling.
Proteins that bind specific drugs with high affinity and trigger intracellular changes influencing the behavior of cells. Drug receptors are generally thought to be receptors for some endogenous substance not otherwise specified.
The degree of similarity between sequences of amino acids. This information is useful for the analyzing genetic relatedness of proteins and species.
A dihydropyridine calcium antagonist with positive inotropic effects. It lowers blood pressure by reducing peripheral vascular resistance through a highly selective action on smooth muscle in arteriolar resistance vessels.
Genetically engineered MUTAGENESIS at a specific site in the DNA molecule that introduces a base substitution, or an insertion or deletion.
ATP-BINDING CASSETTE PROTEINS that are highly conserved and widely expressed in nature. They form an integral part of the ATP-sensitive potassium channel complex which has two intracellular nucleotide folds that bind to sulfonylureas and their analogs.
Unstriated and unstriped muscle, one of the muscles of the internal organs, blood vessels, hair follicles, etc. Contractile elements are elongated, usually spindle-shaped cells with centrally located nuclei. Smooth muscle fibers are bound together into sheets or bundles by reticular fibers and frequently elastic nets are also abundant. (From Stedman, 25th ed)
The part of brain that lies behind the BRAIN STEM in the posterior base of skull (CRANIAL FOSSA, POSTERIOR). It is also known as the "little brain" with convolutions similar to those of CEREBRAL CORTEX, inner white matter, and deep cerebellar nuclei. Its function is to coordinate voluntary movements, maintain balance, and learn motor skills.
A subfamily in the family MURIDAE, comprising the hamsters. Four of the more common genera are Cricetus, CRICETULUS; MESOCRICETUS; and PHODOPUS.
The excitable plasma membrane of a muscle cell. (Glick, Glossary of Biochemistry and Molecular Biology, 1990)
The part of CENTRAL NERVOUS SYSTEM that is contained within the skull (CRANIUM). Arising from the NEURAL TUBE, the embryonic brain is comprised of three major parts including PROSENCEPHALON (the forebrain); MESENCEPHALON (the midbrain); and RHOMBENCEPHALON (the hindbrain). The developed brain consists of CEREBRUM; CEREBELLUM; and other structures in the BRAIN STEM.
A voltage-gated sodium channel subtype that mediates the sodium ion PERMEABILITY of SKELETAL MYOCYTES. Defects in the SCN4A gene, which codes for the alpha subunit of this sodium channel, are associated with several MYOTONIC DISORDERS.
A family of voltage-gated eukaryotic porins that form aqueous channels. They play an essential role in mitochondrial CELL MEMBRANE PERMEABILITY, are often regulated by BCL-2 PROTO-ONCOGENE PROTEINS, and have been implicated in APOPTOSIS.
The processes whereby the internal environment of an organism tends to remain balanced and stable.
Interstitial space between cells, occupied by INTERSTITIAL FLUID as well as amorphous and fibrous substances. For organisms with a CELL WALL, the extracellular space includes everything outside of the CELL MEMBRANE including the PERIPLASM and the cell wall.
The domestic dog, Canis familiaris, comprising about 400 breeds, of the carnivore family CANIDAE. They are worldwide in distribution and live in association with people. (Walker's Mammals of the World, 5th ed, p1065)
A proline analog that acts as a stoichiometric replacement of proline. It causes the production of abnormal proteins with impaired biological activity.
Cellular release of material within membrane-limited vesicles by fusion of the vesicles with the CELL MEMBRANE.
One of the two major classes of cholinergic receptors. Nicotinic receptors were originally distinguished by their preference for NICOTINE over MUSCARINE. They are generally divided into muscle-type and neuronal-type (previously ganglionic) based on pharmacology, and subunit composition of the receptors.
The lower right and left chambers of the heart. The right ventricle pumps venous BLOOD into the LUNGS and the left ventricle pumps oxygenated blood into the systemic arterial circulation.

Functional consequences of mutations in the human alpha1A calcium channel subunit linked to familial hemiplegic migraine. (1/8682)

Mutations in alpha1A, the pore-forming subunit of P/Q-type calcium channels, are linked to several human diseases, including familial hemiplegic migraine (FHM). We introduced the four missense mutations linked to FHM into human alpha1A-2 subunits and investigated their functional consequences after expression in human embryonic kidney 293 cells. By combining single-channel and whole-cell patch-clamp recordings, we show that all four mutations affect both the biophysical properties and the density of functional channels. Mutation R192Q in the S4 segment of domain I increased the density of functional P/Q-type channels and their open probability. Mutation T666M in the pore loop of domain II decreased both the density of functional channels and their unitary conductance (from 20 to 11 pS). Mutations V714A and I1815L in the S6 segments of domains II and IV shifted the voltage range of activation toward more negative voltages, increased both the open probability and the rate of recovery from inactivation, and decreased the density of functional channels. Mutation V714A decreased the single-channel conductance to 16 pS. Strikingly, the reduction in single-channel conductance induced by mutations T666M and V714A was not observed in some patches or periods of activity, suggesting that the abnormal channel may switch on and off, perhaps depending on some unknown factor. Our data show that the FHM mutations can lead to both gain- and loss-of-function of human P/Q-type calcium channels.  (+info)

Ionic currents underlying spontaneous action potentials in isolated cerebellar Purkinje neurons. (2/8682)

Acutely dissociated cell bodies of mouse Purkinje neurons spontaneously fired action potentials at approximately 50 Hz (25 degrees C). To directly measure the ionic currents underlying spontaneous activity, we voltage-clamped the cells using prerecorded spontaneous action potentials (spike trains) as voltage commands and used ionic substitution and selective blockers to isolate individual currents. The largest current flowing during the interspike interval was tetrodotoxin-sensitive sodium current (approximately -50 pA between -65 and -60 mV). Although the neurons had large voltage-dependent calcium currents, the net current blocked by cobalt substitution for calcium was outward at all times during spike trains. Thus, the electrical effect of calcium current is apparently dominated by rapidly activated calcium-dependent potassium currents. Under current clamp, all cells continued firing spontaneously (though approximately 30% more slowly) after block of T-type calcium current by mibefradil, and most cells continued to fire after block of all calcium current by cobalt substitution. Although the neurons possessed hyperpolarization-activated cation current (Ih), little current flowed during spike trains, and block by 1 mM cesium had no effect on firing frequency. The outward potassium currents underlying the repolarization of the spikes were completely blocked by 1 mM TEA. These currents deactivated quickly (<1 msec) after each spike. We conclude that the spontaneous firing of Purkinje neuron cell bodies depends mainly on tetrodotoxin-sensitive sodium current flowing between spikes. The high firing rate is promoted by large potassium currents that repolarize the cell rapidly and deactivate quickly, thus preventing strong hyperpolarization and restoring a high input resistance for subsequent depolarization.  (+info)

Somatic recording of GABAergic autoreceptor current in cerebellar stellate and basket cells. (3/8682)

Patch-clamp recordings were performed from stellate and basket cells in rat cerebellar slices. Under somatic voltage clamp, short depolarizing pulses were applied to elicit action potentials in the axon. After the action potential, a bicuculline- and Cd2+-sensitive current transient was observed. A similar response was obtained when eliciting axonal firing by extracellular stimulation. With an isotonic internal Cl- solution, the peak amplitude of this current varied linearly with the holding potential, yielding an extrapolated reversal potential of -20 to 0 mV. Unlike synaptic or autaptic GABAergic currents obtained in the same preparation, the current transient had a slow rise-time and a low variability between trials. This current was blocked when 10 mM BAPTA was included in the recording solution. In some experiments, the current transient elicited axonal action potentials. The current transient was reliably observed in animals aged 12-15 d, with a mean amplitude of 82 pA at -70 mV, but was small and rare in the age group 29-49 d. Numerical simulations could account for all properties of the current transient by assuming that an action potential activates a distributed GABAergic conductance in the axon. The actual conductance is probably restricted to release sites, with an estimated mean presynaptic current response of 10 pA per site (-70 mV, age 12-15 d). We conclude that in developing rats, stellate and basket cell axons have a high density of GABAergic autoreceptors and that a sizable fraction of the corresponding current can be measured from the soma.  (+info)

Activation of human D3 dopamine receptor inhibits P/Q-type calcium channels and secretory activity in AtT-20 cells. (4/8682)

The D3 dopamine receptor is postulated to play an important role in the regulation of neurotransmitter secretion at both pre- and postsynaptic terminals. However, this hypothesis and the underlying mechanisms remain untested because of the lack of D3-selective ligands, paucity of appropriate model secretory systems, and the weak and inconsistent coupling of D3 receptors to classical signal transduction pathways. The absence of ligands that selectively discriminate between D3 and D2 receptors in vivo precludes the study of D3 receptor function in the brain and necessitates the use of heterologous expression systems. In this report we demonstrate that activation of the human D3 dopamine receptor expressed in the AtT-20 neuroendocrine cell line causes robust inhibition of P/Q-type calcium channels via pertussis toxin-sensitive G-proteins. In addition, using the vesicle trafficking dye FM1-43, we show that D3 receptor activation significantly inhibits spontaneous secretory activity in these cells. Our results not only support the hypothesis that the D3 receptor can regulate secretory activity but also provide insight into the underlying signaling mechanisms. We propose a functional model in which the D3 receptor tightly regulates neurotransmitter release at a synapse by only allowing the propagation of spikes above a certain frequency or burst-duration threshold.  (+info)

Voltage and calcium use the same molecular determinants to inactivate calcium channels. (5/8682)

During sustained depolarization, voltage-gated Ca2+ channels progressively undergo a transition to a nonconducting, inactivated state, preventing Ca2+ overload of the cell. This transition can be triggered either by the membrane potential (voltage-dependent inactivation) or by the consecutive entry of Ca2+ (Ca2+-dependent inactivation), depending on the type of Ca2+ channel. These two types of inactivation are suspected to arise from distinct underlying mechanisms, relying on specific molecular sequences of the different pore-forming Ca2+ channel subunits. Here we report that the voltage-dependent inactivation (of the alpha1A Ca2+ channel) and the Ca2+-dependent inactivation (of the alpha1C Ca2+ channel) are similarly influenced by Ca2+ channel beta subunits. The same molecular determinants of the beta subunit, and therefore the same subunit interactions, influence both types of inactivation. These results strongly suggest that the voltage and the Ca2+-dependent transitions leading to channel inactivation use homologous structures of the different alpha1 subunits and occur through the same molecular process. A model of inactivation taking into account these new data is presented.  (+info)

Calmodulin mediates calcium-dependent activation of the intermediate conductance KCa channel, IKCa1. (6/8682)

Small and intermediate conductance Ca2+-activated K+ channels play a crucial role in hyperpolarizing the membrane potential of excitable and nonexcitable cells. These channels are exquisitely sensitive to cytoplasmic Ca2+, yet their protein-coding regions do not contain consensus Ca2+-binding motifs. We investigated the involvement of an accessory protein in the Ca2+-dependent gating of hIKCa1, a human intermediate conductance channel expressed in peripheral tissues. Cal- modulin was found to interact strongly with the cytoplasmic carboxyl (C)-tail of hIKCa1 in a yeast two-hybrid system. Deletion analyses defined a requirement for the first 62 amino acids of the C-tail, and the binding of calmodulin to this region did not require Ca2+. The C-tail of hSKCa3, a human neuronal small conductance channel, also bound calmodulin, whereas that of a voltage-gated K+ channel, mKv1.3, did not. Calmodulin co-precipitated with the channel in cell lines transfected with hIKCa1, but not with mKv1. 3-transfected lines. A mutant calmodulin, defective in Ca2+ sensing but retaining binding to the channel, dramatically reduced current amplitudes when co-expressed with hIKCa1 in mammalian cells. Co-expression with varying amounts of wild-type and mutant calmodulin resulted in a dominant-negative suppression of current, consistent with four calmodulin molecules being associated with the channel. Taken together, our results suggest that Ca2+-calmodulin-induced conformational changes in all four subunits are necessary for the channel to open.  (+info)

Characterization of elementary Ca2+ release signals in NGF-differentiated PC12 cells and hippocampal neurons. (7/8682)

Elementary Ca2+ release signals in nerve growth factor- (NGF-) differentiated PC12 cells and hippocampal neurons, functionally analogous to the "Ca2+ sparks" and "Ca2+ puffs" identified in other cell types, were characterized by confocal microscopy. They either occurred spontaneously or could be activated by caffeine and metabotropic agonists. The release events were dissimilar to the sparks and puffs described so far, as many arose from clusters of both ryanodine receptors (RyRs) and inositol 1,4,5-trisphosphate receptors (InsP3Rs). Increasing either the stimulus strength or loading of the intracellular stores enhanced the frequency of and coupling between elementary release sites and evoked global Ca2+ signals. In the PC12 cells, the elementary Ca2+ release preferentially occurred around the branch points. Spatio-temporal recruitment of such elementary release events may regulate neuronal activities.  (+info)

Control and assessment of the uterus and cervix during pregnancy and labour. (8/8682)

Preterm labour and resultant preterm birth are the most important problems in perinatology. Countless efforts have failed to establish a single effective treatment of preterm labour, partly because the mechanisms regulating the uterus and cervix during pregnancy are not well understood. New knowledge is needed to inhibit early progression of labour (uterine contractility and cervical ripening), and adequate quantitative tools to evaluate the uterus and cervix during pregnancy are lacking. In this review, we outline studies showing that the uterus (myometrium) and cervix pass through a conditioning step in preparation for labour. This step is not easily identifiable with present methods to assess the uterus or cervix. In the uterus, this seemingly irreversible step consists of changes in the electrical properties to make muscle more excitable and responsive to produce forceful contractions. In the cervix, the step consists of softening of the connective tissue components. Progesterone appears to have a dominant role in controlling both the uterus and cervix, as antiprogestins induce early, preterm conditioning leading to preterm labour. Apparently, nitric oxide (NO) also controls conditioning of the uterus and cervix. In the uterus, NO, in concert with progesterone, inhibits uterine contractility. At term, NO production by the uterus and placenta are decreased and allow labour to progress. In contrast, NO in the cervix increases at the end of pregnancy and it may be the final pathway for stimulating cervical ripening by activation of metalloenzymes. The progress of labour can be assessed non-invasively using electromyographic (EMG) signals from the uterus (the driving force for contractility) recorded from the abdominal surface. Uterine EMG bursts detected in this manner characterize uterine contractile events during human and animal pregnancy. A low uterine EMG activity, measured transabdominally throughout most of pregnancy, rises dramatically during labour. EMG activity also increases substantially during preterm labour in humans and rats. This method may be used one day to predict impending preterm labour and identify control steps and treatments. A quantitative method also assesses the cervix, using an optical device which measures collagen fluorescence in the cervix. The collascope estimates cervical collagen content from a fluorescent signal generated when collagen cross-links are illuminated with excitation light of about 340 nm. The system has proved useful in rats and humans at various stages of pregnancy, and indicates that cervical softening occurs progressively in the last one-third of pregnancy. In rats, collascope readings correlate with resistance measurements made in the isolated cervix, which may help to assess cervical function during pregnancy, and indicate control and treatments.  (+info)

There are several types of channelopathies, including:

1. Long QT syndrome: This is a condition that affects the ion channels in the heart, leading to abnormal heart rhythms and increased risk of sudden death.
2. Short QT syndrome: This is a rare condition that has the opposite effect of long QT syndrome, causing the heart to beat too quickly.
3. Catecholaminergic polymorphic ventricular tachycardia (CPVT): This is a rare disorder that affects the ion channels in the heart, leading to abnormal heart rhythms and increased risk of sudden death.
4. Brugada syndrome: This is a condition that affects the ion channels in the heart, leading to abnormal heart rhythms and increased risk of sudden death.
5. Wolff-Parkinson-White (WPW) syndrome: This is a condition that affects the ion channels in the heart, leading to abnormal heart rhythms and increased risk of sudden death.
6. Neuromuscular disorders: These are disorders that affect the nerve-muscle junction, leading to muscle weakness and wasting. Examples include muscular dystrophy and myasthenia gravis.
7. Dystrophinopathies: These are a group of disorders that affect the structure of muscle cells, leading to muscle weakness and wasting. Examples include Duchenne muscular dystrophy and Becker muscular dystrophy.
8. Myotonia: This is a condition that affects the muscles, causing them to become stiff and rigid.
9. Hyperkalemic periodic paralysis: This is a rare condition that causes muscle weakness and paralysis due to abnormal potassium levels in the body.
10. Hypokalemic periodic paralysis: This is a rare condition that causes muscle weakness and paralysis due to low potassium levels in the body.
11. Thyrotoxic periodic paralysis: This is a rare condition that causes muscle weakness and paralysis due to an overactive thyroid gland.
12. Hyperthyroidism: This is a condition where the thyroid gland becomes overactive, leading to increased heart rate, weight loss, and muscle weakness.
13. Hypothyroidism: This is a condition where the thyroid gland becomes underactive, leading to fatigue, weight gain, and muscle weakness.
14. Pituitary tumors: These are tumors that affect the pituitary gland, which regulates hormone production in the body.
15. Adrenal tumors: These are tumors that affect the adrenal glands, which produce hormones such as cortisol and aldosterone.
16. Carcinoid syndrome: This is a condition where cancer cells in the digestive system produce hormones that can cause muscle weakness and wasting.
17. Multiple endocrine neoplasia (MEN): This is a genetic disorder that affects the endocrine system and can cause tumors to grow in the thyroid, adrenal, and parathyroid glands.

These are just some of the many potential causes of muscle weakness. It's important to see a healthcare professional for an accurate diagnosis and appropriate treatment.

There are two types of hypertension:

1. Primary Hypertension: This type of hypertension has no identifiable cause and is also known as essential hypertension. It accounts for about 90% of all cases of hypertension.
2. Secondary Hypertension: This type of hypertension is caused by an underlying medical condition or medication. It accounts for about 10% of all cases of hypertension.

Some common causes of secondary hypertension include:

* Kidney disease
* Adrenal gland disorders
* Hormonal imbalances
* Certain medications
* Sleep apnea
* Cocaine use

There are also several risk factors for hypertension, including:

* Age (the risk increases with age)
* Family history of hypertension
* Obesity
* Lack of exercise
* High sodium intake
* Low potassium intake
* Stress

Hypertension is often asymptomatic, and it can cause damage to the blood vessels and organs over time. Some potential complications of hypertension include:

* Heart disease (e.g., heart attacks, heart failure)
* Stroke
* Kidney disease (e.g., chronic kidney disease, end-stage renal disease)
* Vision loss (e.g., retinopathy)
* Peripheral artery disease

Hypertension is typically diagnosed through blood pressure readings taken over a period of time. Treatment for hypertension may include lifestyle changes (e.g., diet, exercise, stress management), medications, or a combination of both. The goal of treatment is to reduce the risk of complications and improve quality of life.

The symptoms of LEMS typically develop gradually over time and may include:

1. Muscle weakness that worsens with activity and improves with rest.
2. Weakness in the legs, hips, and shoulders.
3. Fatigue and muscle cramps.
4. Difficulty walking or standing upright.
5. Double vision or other eye problems.
6. Dry mouth and difficulty swallowing.
7. Increased heart rate and blood pressure.
8. Impaired reflexes.
9. Decreased sweating.
10. Weight loss.

The exact cause of LEMS is not known, but it is believed to be an autoimmune disorder in which the immune system mistakenly attacks the VGCCs in the neuromuscular junction. The condition is often associated with other autoimmune disorders such as thyroiditis, vitiligo, and adrenal insufficiency.

There is no cure for LEMS, but treatment options are available to manage the symptoms. These may include:

1. Immunosuppressive medications such as prednisone to reduce inflammation and suppress the immune system.
2. Intracranial pressure-lowering medications such as acetazolamide to reduce the pressure in the brain.
3. Muscle strengthening exercises to improve muscle function.
4. Physical therapy to maintain muscle strength and flexibility.
5. Orthostatic hypotension medications to manage orthostatic hypotension (a drop in blood pressure when standing).
6. Pain management medications to relieve muscle cramps, spasms, or pain.
7. Nutritional support to ensure adequate nutrition and prevent weight loss.
8. Respiratory support as needed to manage respiratory muscle weakness.
9. Speech therapy to improve communication skills.
10. Psychological support to cope with the emotional and social challenges of the condition.

It is important for individuals with LEMS to work closely with their healthcare team to manage their symptoms and prevent complications. With proper treatment, many people with LEMS can lead active and fulfilling lives.

The diagnosis of absence epilepsy is typically made based on a combination of clinical findings, including:
-A history of recurrent brief loss of awareness or staring spells
-Normal neurological examination between episodes
-Abnormal EEG activity during seizures (spikes or sharp waves)

Treatment for absence epilepsy usually involves medication, such as ethosuximide, valproic acid, or lamotrigine. In some cases, surgery may be considered if medications are ineffective or have significant side effects.

It is important to note that absence epilepsy can be a challenging condition to diagnose and treat, as the spells can be difficult to distinguish from other conditions such as daydreaming or attention deficit hyperactivity disorder (ADHD).

Some common types of calcium metabolism disorders include:

1. Hypocalcemia (low calcium levels): This can be caused by a deficiency in dietary calcium intake, malabsorption of calcium, or excessive urinary excretion of calcium. Symptoms can include muscle cramps, tremors, and tingling sensations in the fingers and toes.
2. Hypercalcemia (high calcium levels): This can be caused by an overactive parathyroid gland, cancer, or excessive intake of vitamin D. Symptoms can include fatigue, nausea, constipation, and kidney stones.
3. Osteoporosis: This is a condition characterized by weak and brittle bones that can lead to fractures. It is often associated with hormonal imbalances, vitamin D deficiency, or other factors that disrupt calcium metabolism.
4. Hyperparathyroidism (overactive parathyroid gland): This is a condition in which the parathyroid glands produce too much parathyroid hormone (PTH), leading to elevated calcium levels and potential complications such as kidney stones, bone loss, and cardiovascular disease.
5. Vitamin D-dependent rickets type 1: This is a rare genetic disorder that affects the body's ability to absorb vitamin D and maintain normal calcium levels. It can lead to softening of the bones and other skeletal deformities.
6. Familial hypophosphatemic rickets type 1: This is a rare genetic disorder that affects the body's ability to regulate phosphate levels, leading to softening of the bones and other skeletal deformities.
7. Tumor-induced osteomalacia: This is a condition in which cancerous tumors, typically found in the lung or breast, produce high levels of proteins that interfere with the body's ability to absorb vitamin D and maintain normal calcium levels. It can lead to softening of the bones and other skeletal deformities.
8. Chronic kidney disease: This is a condition in which the kidneys are not functioning properly, leading to elevated levels of phosphate and other waste products in the blood. It can lead to softening of the bones and other complications such as heart disease.
9. Paget's disease of bone: This is a condition that affects the way bones grow and repair themselves, leading to deformities and pain. It is often associated with inflammation and elevated levels of calcium in the blood.
10. Chronic alcoholism: Prolonged heavy drinking can lead to deficiencies in vitamin D and calcium, as well as other nutrients that are essential for bone health. It can increase the risk of osteoporosis and fractures.

1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.

2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.

3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.

4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.

5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.

6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.

7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.

8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.

9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.

10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.

The QT interval is a measure of the time it takes for the ventricles to recover from each heartbeat and prepare for the next one. In people with LQTS, this recovery time is prolonged, which can disrupt the normal rhythm of the heart and increase the risk of arrhythmias.

LQTS is caused by mutations in genes that encode proteins involved in the cardiac ion channels, which regulate the flow of ions into and out of the heart muscle cells. These mutations can affect the normal functioning of the ion channels, leading to abnormalities in the electrical activity of the heart.

Symptoms of LQTS can include palpitations, fainting spells, and seizures. In some cases, LQTS can be diagnosed based on a family history of the condition or after a sudden death in an otherwise healthy individual. Other tests, such as an electrocardiogram (ECG), echocardiogram, and stress test, may also be used to confirm the diagnosis.

Treatment for LQTS typically involves medications that regulate the heart's rhythm and reduce the risk of arrhythmias. In some cases, an implantable cardioverter-defibrillator (ICD) may be recommended to monitor the heart's activity and deliver an electric shock if a potentially life-threatening arrhythmia is detected. Lifestyle modifications, such as avoiding stimuli that trigger symptoms and taking precautions during exercise and stress, may also be recommended.

In summary, Long QT syndrome is a rare inherited disorder that affects the electrical activity of the heart, leading to an abnormal prolongation of the QT interval and an increased risk of irregular and potentially life-threatening heart rhythms. It is important for individuals with LQTS to be closely monitored by a healthcare provider and to take precautions to manage their condition and reduce the risk of complications.

There are several types of kidney calculi, including:

1. Calcium oxalate calculi: These are the most common type of calculus and are often associated with conditions such as hyperparathyroidism or excessive intake of calcium supplements.
2. Uric acid calculi: These are more common in people with gout or a diet high in meat and sugar.
3. Cystine calculi: These are rare and usually associated with a genetic disorder called cystinuria.
4. Struvite calculi: These are often seen in women with urinary tract infections (UTIs).

Symptoms of kidney calculi may include:

1. Flank pain (pain in the side or back)
2. Pain while urinating
3. Blood in the urine
4. Cloudy or strong-smelling urine
5. Fever and chills
6. Nausea and vomiting

Kidney calculi are diagnosed through a combination of physical examination, medical history, and diagnostic tests such as X-rays, CT scans, or ultrasound. Treatment options for kidney calculi depend on the size and location of the calculus, as well as the severity of any underlying conditions. Small calculi may be treated with conservative measures such as fluid intake and medication to help flush out the crystals, while larger calculi may require surgical intervention to remove them.

Preventive measures for kidney calculi include staying hydrated to help flush out excess minerals in the urine, maintaining a balanced diet low in oxalate and animal protein, and avoiding certain medications that can increase the risk of calculus formation. Early detection and treatment of underlying conditions such as hyperparathyroidism or gout can also help prevent the development of kidney calculi.

Overall, kidney calculi are a common condition that can be managed with proper diagnosis and treatment. However, they can cause significant discomfort and potentially lead to complications if left untreated, so it is important to seek medical attention if symptoms persist or worsen over time.

The symptoms of hypokalemic periodic paralysis can vary in severity and may include:

* Muscle weakness or paralysis, typically affecting the legs but sometimes affecting the arms or face as well
* Muscle cramps and twitching
* Abnormal heart rhythms
* Weakness or paralysis of the respiratory muscles, which can lead to breathing difficulties
* Vision problems, such as blurred vision or double vision
* Dizziness and fainting

The exact cause of hypokalemic periodic paralysis is not known, but it is thought to be related to mutations in certain genes that affect the way potassium ions are regulated in the body. The disorder is usually diagnosed through a combination of clinical evaluation, laboratory tests, and genetic analysis.

There is no cure for hypokalemic periodic paralysis, but treatment options may include:

* Potassium supplements to maintain normal potassium levels in the blood
* Medications to regulate heart rhythms and prevent abnormal heartbeats
* Physical therapy to improve muscle strength and function
* Avoiding triggers such as stress, certain medications, or changes in potassium levels
* In severe cases, a pacemaker may be implanted to regulate the heartbeat.

It is important to note that hypokalemic periodic paralysis can be a challenging disorder to manage and may have a significant impact on quality of life. However, with proper treatment and management, many individuals with this condition are able to lead active and fulfilling lives.

Some common causes of hypocalcemia include:

1. Vitamin D deficiency: Vitamin D is essential for the absorption of calcium from the diet. A lack of vitamin D can lead to low levels of calcium in the blood.
2. Parathyroid gland disorders: The parathyroid glands are located in the neck and regulate calcium levels in the blood. Disorders such as hypoparathyroidism (underactive parathyroid glands) or hyperparathyroidism (overactive parathyroid glands) can cause hypocalcemia.
3. Malabsorption: Certain conditions, such as celiac disease or Crohn's disease, can lead to malabsorption of nutrients, including calcium.
4. Kidney problems: Kidney failure can cause hypocalcemia by reducing the amount of calcium that is excreted in the urine.
5. Hypomagnesemia (low levels of magnesium): Magnesium is important for calcium metabolism, and low levels of magnesium can contribute to hypocalcemia.

Symptoms of hypocalcemia can include:

1. Muscle cramps
2. Weakness
3. Twitching or tremors
4. Seizures
5. Tingling or numbness in the fingers and toes
6. Difficulty swallowing
7. Palpitations
8. Headaches
9. Fatigue
10. Depression

Treatment for hypocalcemia usually involves addressing the underlying cause of the condition. For example, if the condition is caused by a vitamin D deficiency, supplements may be prescribed. If the condition is caused by a parathyroid gland disorder, surgery may be necessary to remove the affected gland or glands. In some cases, calcium supplements may be prescribed to help restore normal calcium levels.

It's important to note that hypocalcemia can be a sign of an underlying condition, and it should be treated promptly to prevent complications. If you suspect you or someone you know may have hypocalcemia, it is important to seek medical attention as soon as possible. A healthcare professional can diagnose the condition and recommend appropriate treatment.


* Genetic mutations or deletions
* Infections such as meningitis or encephalitis
* Stroke or bleeding in the brain
* Traumatic head injury
* Multiple sclerosis or other demyelinating diseases
* Brain tumors
* Cerebellar degeneration due to aging


* Coordination difficulties, such as stumbling or poor balance
* Tremors or shaky movements
* Slurred speech and difficulty with fine motor skills
* Nystagmus (involuntary eye movements)
* Difficulty with gait and walking
* Fatigue, weakness, and muscle wasting


* Physical examination and medical history
* Neurological examination to test coordination, balance, and reflexes
* Imaging studies such as MRI or CT scans to rule out other conditions
* Genetic testing to identify inherited forms of cerebellar ataxia
* Electromyography (EMG) to test muscle activity and nerve function


* Physical therapy to improve balance, coordination, and gait
* Occupational therapy to help with daily activities and fine motor skills
* Speech therapy to address slurred speech and communication difficulties
* Medications to manage symptoms such as tremors or spasticity
* Assistive devices such as canes or walkers to improve mobility


* The prognosis for cerebellar ataxia varies depending on the underlying cause. In some cases, the condition may be slowly progressive and lead to significant disability over time. In other cases, the condition may remain stable or even improve with treatment.

Living with cerebellar ataxia can be challenging, but there are many resources available to help individuals with the condition manage their symptoms and maintain their quality of life. These resources may include:

* Physical therapy to improve balance and coordination
* Occupational therapy to assist with daily activities
* Speech therapy to address communication difficulties
* Assistive devices such as canes or walkers to improve mobility
* Medications to manage symptoms such as tremors or spasticity
* Support groups for individuals with cerebellar ataxia and their families

Overall, the key to managing cerebellar ataxia is early diagnosis and aggressive treatment. With proper management, individuals with this condition can lead active and fulfilling lives despite the challenges they face.

There are many different types of cardiac arrhythmias, including:

1. Tachycardias: These are fast heart rhythms that can be too fast for the body's needs. Examples include atrial fibrillation and ventricular tachycardia.
2. Bradycardias: These are slow heart rhythms that can cause symptoms like fatigue, dizziness, and fainting. Examples include sinus bradycardia and heart block.
3. Premature beats: These are extra beats that occur before the next regular beat should come in. They can be benign but can also indicate an underlying arrhythmia.
4. Supraventricular arrhythmias: These are arrhythmias that originate above the ventricles, such as atrial fibrillation and paroxysmal atrial tachycardia.
5. Ventricular arrhythmias: These are arrhythmias that originate in the ventricles, such as ventricular tachycardia and ventricular fibrillation.

Cardiac arrhythmias can be diagnosed through a variety of tests including electrocardiograms (ECGs), stress tests, and holter monitors. Treatment options for cardiac arrhythmias vary depending on the type and severity of the condition and may include medications, cardioversion, catheter ablation, or implantable devices like pacemakers or defibrillators.

The symptoms of hypercalcemia may include:

* Fatigue
* Nausea and vomiting
* Weakness
* Constipation
* Abdominal pain
* Kidney stones
* Bone pain or fractures

If left untreated, hypercalcemia can lead to complications such as kidney damage, heart problems, and an increased risk of osteoporosis. Treatment options may include medications to reduce calcium levels, surgery to remove a tumor or overactive parathyroid gland, or dialysis if the patient has kidney failure.

Early diagnosis and treatment are important to prevent long-term complications and improve the patient's quality of life.

Neuroblastoma is caused by a genetic mutation that affects the development and growth of nerve cells. The cancerous cells are often sensitive to chemotherapy, but they can be difficult to remove surgically because they are deeply embedded in the nervous system.

There are several different types of neuroblastoma, including:

1. Infantile neuroblastoma: This type of neuroblastoma occurs in children under the age of one and is often more aggressive than other types of the cancer.
2. Juvenile neuroblastoma: This type of neuroblastoma occurs in children between the ages of one and five and tends to be less aggressive than infantile neuroblastoma.
3. Adult neuroblastoma: This type of neuroblastoma occurs in adults and is rare.
4. Metastatic neuroblastoma: This type of neuroblastoma has spread to other parts of the body, such as the bones or liver.

Symptoms of neuroblastoma can vary depending on the location and size of the tumor, but they may include:

* Abdominal pain
* Fever
* Loss of appetite
* Weight loss
* Fatigue
* Bone pain
* Swelling in the abdomen or neck
* Constipation
* Increased heart rate

Diagnosis of neuroblastoma typically involves a combination of imaging tests, such as CT scans and MRI scans, and biopsies to confirm the presence of cancerous cells. Treatment for neuroblastoma usually involves a combination of chemotherapy, surgery, and radiation therapy. The prognosis for neuroblastoma varies depending on the type of cancer, the age of the child, and the stage of the disease. In general, the younger the child and the more aggressive the treatment, the better the prognosis.

Neuralgia is often difficult to diagnose and treat, as the underlying cause can be challenging to identify. However, various medications and therapies can help manage the pain and other symptoms associated with this condition. These may include pain relievers, anticonvulsants, antidepressants, and muscle relaxants, as well as alternative therapies such as acupuncture or physical therapy.

Some common forms of neuralgia include:

1. Trigeminal neuralgia: This is a condition that affects the trigeminal nerve, which carries sensation from the face to the brain. It is characterized by sudden, intense pain in the face, typically on one side.
2. Postherpetic neuralgia (PHN): This is a condition that occurs after a shingles infection, and is characterized by persistent pain in the affected area.
3. Occipital neuralgia: This is a condition that affects the nerves in the back of the head and neck, and can cause pain in the back of the head, neck, and face.
4. Geniculate neuralgia: This is a rare condition that affects the nerves in the jaw and ear, and can cause pain in the jaw, face, and ear.

Overall, neuralgia is a complex and debilitating condition that can significantly impact an individual's quality of life. It is important for individuals experiencing symptoms of neuralgia to seek medical attention to determine the underlying cause and develop an appropriate treatment plan.

There are several types of ataxia, each with different symptoms and causes. Some common forms of ataxia include:

1. Spinocerebellar ataxia (SCA): This is the most common form of ataxia and is caused by a degeneration of the cerebellum and spinal cord. It can cause progressive weakness, loss of coordination, and difficulty with speaking and swallowing.
2. Friedreich's ataxia: This is the second most common form of ataxia and is caused by a deficiency of vitamin E in the body. It can cause weakness in the legs, difficulty walking, and problems with speech and language.
3. Ataxia-telangiectasia (AT): This is a rare form of ataxia that is caused by a gene mutation. It can cause progressive weakness, loss of coordination, and an increased risk of developing cancer.
4. Acute cerebellar ataxia: This is a sudden and temporary form of ataxia that can be caused by a variety of factors such as infections, injuries, or certain medications.
5. Drug-induced ataxia: Certain medications can cause ataxia as a side effect.
6. Vitamin deficiency ataxia: Deficiencies in vitamins such as vitamin B12 or folate can cause ataxia.
7. Metabolic disorders: Certain metabolic disorders such as hypothyroidism, hyperthyroidism, and hypoglycemia can cause ataxia.
8. Stroke or brain injury: Ataxia can be a result of a stroke or brain injury.
9. Multiple system atrophy (MSA): This is a rare progressive neurodegenerative disorder that can cause ataxia, parkinsonism, and autonomic dysfunction.
10. Spinocerebellar ataxia (SCA): This is a group of rare genetic disorders that can cause progressive cerebellar ataxia, muscle wasting, and other signs and symptoms.

It's important to note that this is not an exhaustive list and there may be other causes of ataxia not mentioned here. If you suspect you or someone you know may have ataxia, it is important to consult a healthcare professional for proper diagnosis and treatment.

There are several different types of pain, including:

1. Acute pain: This type of pain is sudden and severe, and it usually lasts for a short period of time. It can be caused by injuries, surgery, or other forms of tissue damage.
2. Chronic pain: This type of pain persists over a long period of time, often lasting more than 3 months. It can be caused by conditions such as arthritis, fibromyalgia, or nerve damage.
3. Neuropathic pain: This type of pain results from damage to the nervous system, and it can be characterized by burning, shooting, or stabbing sensations.
4. Visceral pain: This type of pain originates in the internal organs, and it can be difficult to localize.
5. Psychogenic pain: This type of pain is caused by psychological factors such as stress, anxiety, or depression.

The medical field uses a range of methods to assess and manage pain, including:

1. Pain rating scales: These are numerical scales that patients use to rate the intensity of their pain.
2. Pain diaries: These are records that patients keep to track their pain over time.
3. Clinical interviews: Healthcare providers use these to gather information about the patient's pain experience and other relevant symptoms.
4. Physical examination: This can help healthcare providers identify any underlying causes of pain, such as injuries or inflammation.
5. Imaging studies: These can be used to visualize the body and identify any structural abnormalities that may be contributing to the patient's pain.
6. Medications: There are a wide range of medications available to treat pain, including analgesics, nonsteroidal anti-inflammatory drugs (NSAIDs), and muscle relaxants.
7. Alternative therapies: These can include acupuncture, massage, and physical therapy.
8. Interventional procedures: These are minimally invasive procedures that can be used to treat pain, such as nerve blocks and spinal cord stimulation.

It is important for healthcare providers to approach pain management with a multi-modal approach, using a combination of these methods to address the physical, emotional, and social aspects of pain. By doing so, they can help improve the patient's quality of life and reduce their suffering.

There are several different types of calcinosis, each with its own unique causes and symptoms. Some common forms of calcinosis include:

1. Dystrophic calcinosis: This type of calcinosis occurs in people with muscular dystrophy, a group of genetic disorders that affect muscle strength and function. Dystrophic calcinosis can cause calcium deposits to form in the muscles, leading to muscle weakness and wasting.
2. Metastatic calcinosis: This type of calcinosis occurs when cancer cells spread to other parts of the body and cause calcium deposits to form. Metastatic calcinosis can occur in people with a variety of different types of cancer, including breast, lung, and prostate cancer.
3. Idiopathic calcinosis: This type of calcinosis occurs for no apparent reason, and the exact cause is not known. Idiopathic calcinosis can affect people of all ages and can cause calcium deposits to form in a variety of different tissues.
4. Secondary calcinosis: This type of calcidosis occurs as a result of an underlying medical condition or injury. For example, secondary calcinosis can occur in people with kidney disease, hyperparathyroidism (a condition in which the parathyroid glands produce too much parathyroid hormone), or traumatic injuries.

Treatment for calcinosis depends on the underlying cause and the severity of the condition. In some cases, treatment may involve managing the underlying disease or condition that is causing the calcium deposits to form. Other treatments may include medications to reduce inflammation and pain, physical therapy to improve mobility and strength, and surgery to remove the calcium deposits.

Causes: There are several causes of night blindness, including:

1. Vitamin A deficiency: Vitamin A is essential for the health of the retina, and a deficiency can lead to night blindness.
2. Retinitis pigmentosa: This is a group of inherited conditions that can cause progressive damage to the retina and result in night blindness.
3. Cataracts: A cataract can cause a person to become night blind by blocking the light that enters the eye.
4. Glaucoma: This is a group of eye conditions that can damage the optic nerve and lead to vision loss, including night blindness.
5. Other medical conditions: Certain medical conditions such as diabetes, multiple sclerosis, and stroke can cause night blindness.

Symptoms: The symptoms of night blindness can vary depending on the underlying cause, but common symptoms include:

1. Difficulty seeing in low light environments
2. Blind spots or missing areas of vision
3. Sensitivity to light
4. Glare or halos around lights
5. Difficulty adjusting to changes in light levels

Diagnosis: Night blindness is typically diagnosed through a comprehensive eye exam, which may include a visual acuity test, refraction test, and retinal examination. Imaging tests such as an OCT scan or retinal photography may also be used to evaluate the retina and optic nerve.

Treatment: The treatment of night blindness depends on the underlying cause. For example, vitamin A supplements may be prescribed for a vitamin A deficiency, while cataract surgery may be recommended for cataracts. In some cases, no treatment may be necessary, and the condition may resolve on its own over time.

Prevention: While some cases of night blindness are unavoidable, there are steps you can take to reduce your risk of developing the condition. These include:

1. Maintaining a healthy diet that includes foods rich in vitamin A and other essential nutrients for eye health.
2. Wearing sunglasses with UV protection to protect your eyes from excessive sunlight.
3. Avoiding smoking and excessive alcohol consumption, which can damage the optic nerve and retina.
4. Getting regular eye exams to detect any underlying eye problems early on.
5. Wearing protective eyewear when engaging in activities that could potentially harm your eyes, such as sports or working with hazardous materials.

Migraine with aura is considered to be a more severe form of migraine than migraine without aura, which does not have the same neurological symptoms before the headache. Migraine with aura is also associated with a higher risk of other health problems, such as stroke and dementia.

There are several treatments available for migraine with aura, including medications that can help to reduce the frequency and severity of the headaches, as well as lifestyle changes such as avoiding triggers and getting regular exercise. It is important for people who experience migraine with aura to work closely with their healthcare provider to develop an effective treatment plan.

* Type 1: Hypokalemic Periodic Paralysis (Hyperkalemia-induced muscle weakness)
* Type 2: Hyperkalemic Periodic Paralysis (K+ channels dysfunction, leading to muscle weakness)
* Type 3: Peripheral nerve damage causing FPPA
* Type 4: Central nervous system damage causing FPPA

Slide 3: Causes of Familial Periodic Paralysis (FPPA)

* Genetic mutations in SCN4A, KCNA1, and other genes involved in ion channel function
* Abnormalities in the expression and function of ion channels
* Autosomal dominant or recessive inheritance pattern

Slide 4: Symptoms of Familial Periodic Paralysis (FPPA)

* Muscle weakness or paralysis, often triggered by changes in diet, physical activity, or other environmental factors
* Weakness of the lower extremities more pronounced than the upper extremities
* Muscle cramps and twitching
* Abdominal pain
* Nausea and vomiting

Slide 5: Diagnosis of Familial Periodal Paralysis (FPPA)

* Clinical evaluation, including patient history and physical examination
* Electromyography (EMG) to assess muscle activity and diagnose FPPA
* Genetic testing to identify genetic mutations associated with FPPA
* Blood tests to measure potassium levels and rule out other conditions

Slide 6: Treatment of Familial Periodic Paralysis (FPPA)

* Potassium supplements to maintain normal potassium levels
* Avoiding triggers such as stress, cold temperature, and certain medications
* Physical therapy to improve muscle strength and function
* Pain management with analgesics and other medications as needed

Slide 7: Prognosis of Familial Periodic Paralysis (FPPA)

* FPPA is a chronic condition with no cure, but with proper management, patients can lead relatively normal lives
* The prognosis varies depending on the severity and frequency of attacks, as well as the presence of any complications
* Early diagnosis and treatment can improve the quality of life for patients with FPPA

Slide 8: Current Research in Familial Periodic Paralysis (FPPA)

* Genetic research to better understand the underlying causes of FPPA and develop new treatments
* Studies on the effectiveness of new medications and therapies for FPPA
* Investigation into the potential use of stem cells for treating FPPA

Slide 9: Current Challenges in Familial Periodic Paralysis (FPPA)

* Limited awareness and understanding of FPPA among healthcare professionals and the general public
* Lack of effective treatments for severe cases of FPPA
* Limited availability of specialized care and support for patients with FPPA

Slide 10: Conclusion

* Familial periodic paralysis (FPPA) is a rare and complex condition that affects both children and adults
* Early diagnosis and proper management are critical to improving the quality of life for patients with FPPA
* Ongoing research offers hope for new treatments and therapies, but more work needs to be done to increase awareness and understanding of this condition.

Insulinoma is a rare type of pancreatic tumor that produces excess insulin, leading to low blood sugar levels. These tumors are typically benign and can be treated with surgery or medication.

Insulinomas account for only about 5% of all pancreatic neuroendocrine tumors. They usually occur in the head of the pancreas and can cause a variety of symptoms, including:

1. Hypoglycemia (low blood sugar): The excess insulin produced by the tumor can cause blood sugar levels to drop too low, leading to symptoms such as shakiness, dizziness, confusion, and rapid heartbeat.
2. Hyperinsulinism (elevated insulin levels): In addition to hypoglycemia, insulinomas can also cause elevated insulin levels in the blood.
3. Abdominal pain: Insulinomas can cause abdominal pain and discomfort.
4. Weight loss: Patients with insulinomas may experience unexplained weight loss.
5. Nausea and vomiting: Some patients may experience nausea and vomiting due to the hypoglycemia or other symptoms caused by the tumor.

Insulinomas are usually diagnosed through a combination of imaging tests such as CT scans, MRI scans, and PET scans, and by measuring insulin and C-peptide levels in the blood. Treatment options for insulinomas include surgery to remove the tumor, medications to control hypoglycemia and hyperinsulinism, and somatostatin analogs to reduce hormone secretion.

Insulinoma is a rare and complex condition that requires careful management by a multidisciplinary team of healthcare professionals, including endocrinologists, surgeons, and radiologists. With appropriate treatment, most patients with insulinomas can experience long-term remission and improved quality of life.

Hyperalgesia is often seen in people with chronic pain conditions, such as fibromyalgia, and it can also be a side effect of certain medications or medical procedures. Treatment options for hyperalgesia depend on the underlying cause of the condition, but may include pain management techniques, physical therapy, and medication adjustments.

In clinical settings, hyperalgesia is often assessed using a pinprick test or other pain tolerance tests to determine the patient's sensitivity to different types of stimuli. The goal of treatment is to reduce the patient's pain and improve their quality of life.

There are different types of anoxia, including:

1. Cerebral anoxia: This occurs when the brain does not receive enough oxygen, leading to cognitive impairment, confusion, and loss of consciousness.
2. Pulmonary anoxia: This occurs when the lungs do not receive enough oxygen, leading to shortness of breath, coughing, and chest pain.
3. Cardiac anoxia: This occurs when the heart does not receive enough oxygen, leading to cardiac arrest and potentially death.
4. Global anoxia: This is a complete lack of oxygen to the entire body, leading to widespread tissue damage and death.

Treatment for anoxia depends on the underlying cause and the severity of the condition. In some cases, hospitalization may be necessary to provide oxygen therapy, pain management, and other supportive care. In severe cases, anoxia can lead to long-term disability or death.

Prevention of anoxia is important, and this includes managing underlying medical conditions such as heart disease, diabetes, and respiratory problems. It also involves avoiding activities that can lead to oxygen deprivation, such as scuba diving or high-altitude climbing, without proper training and equipment.

In summary, anoxia is a serious medical condition that occurs when there is a lack of oxygen in the body or specific tissues or organs. It can cause cell death and tissue damage, leading to serious health complications and even death if left untreated. Early diagnosis and treatment are crucial to prevent long-term disability or death.

There are two main types of myotonia:

1. Thomsen's disease: This is an inherited form of myotonia that affects the muscles of the face, neck, and limbs. It is caused by mutations in the CLCN1 gene and can be severe, causing difficulty with speaking, swallowing, and breathing.
2. Becker's muscular dystrophy: This is a form of muscular dystrophy that affects both the skeletal and cardiac muscles. It is caused by mutations in the DMPK gene and can cause myotonia, muscle weakness, and heart problems.

The symptoms of myotonia can vary depending on the severity of the condition and may include:

* Muscle stiffness and rigidity
* Spasms or twitches
* Difficulty with movement and mobility
* Fatigue and weakness
* Cramps
* Muscle wasting

Myotonia can be diagnosed through a combination of physical examination, medical history, and diagnostic tests such as electromyography (EMG) and muscle biopsy. There is no cure for myotonia, but treatment options may include:

* Physical therapy to improve movement and mobility
* Medications to relax muscles and reduce spasms
* Lifestyle modifications such as avoiding triggers and taking regular breaks to rest
* Surgery in severe cases to release or lengthen affected muscles.

It is important to note that myotonia can be a symptom of other underlying conditions, so proper diagnosis and management by a healthcare professional is essential to determine the best course of treatment.

There are many different types of seizures, each with its own unique set of symptoms. Some common types of seizures include:

1. Generalized seizures: These seizures affect both sides of the brain and can cause a range of symptoms, including convulsions, loss of consciousness, and muscle stiffness.
2. Focal seizures: These seizures affect only one part of the brain and can cause more specific symptoms, such as weakness or numbness in a limb, or changes in sensation or vision.
3. Tonic-clonic seizures: These seizures are also known as grand mal seizures and can cause convulsions, loss of consciousness, and muscle stiffness.
4. Absence seizures: These seizures are also known as petit mal seizures and can cause a brief loss of consciousness or staring spell.
5. Myoclonic seizures: These seizures can cause sudden, brief muscle jerks or twitches.
6. Atonic seizures: These seizures can cause a sudden loss of muscle tone, which can lead to falls or drops.
7. Lennox-Gastaut syndrome: This is a rare and severe form of epilepsy that can cause multiple types of seizures, including tonic, atonic, and myoclonic seizures.

Seizures can be diagnosed through a combination of medical history, physical examination, and diagnostic tests such as electroencephalography (EEG) or imaging studies. Treatment for seizures usually involves anticonvulsant medications, but in some cases, surgery or other interventions may be necessary.

Overall, seizures are a complex and multifaceted symptom that can have a significant impact on an individual's quality of life. It is important to seek medical attention if you or someone you know is experiencing seizures, as early diagnosis and treatment can help to improve outcomes and reduce the risk of complications.

The exact cause of malignant hyperthermia is not fully understood, but it is believed to be related to a genetic predisposition and exposure to certain anesthetic agents. The condition can be triggered by a variety of factors, including the use of certain anesthetics, stimulation of the sympathetic nervous system, and changes in blood sugar levels.

Symptoms of malignant hyperthermia can include:

* Elevated body temperature (usually above 104°F/40°C)
* Muscle rigidity and stiffness
* Heart arrhythmias and palpitations
* Shivering or tremors
* Confusion, agitation, or other neurological symptoms
* Shortness of breath or respiratory failure

If left untreated, malignant hyperthermia can lead to serious complications such as seizures, brain damage, and even death. Treatment typically involves the immediate discontinuation of any triggering anesthetic agents, cooling measures such as ice packs or cold compresses, and medications to help regulate body temperature and reduce muscle rigidity. In severe cases, mechanical ventilation may be necessary to support breathing.

Overall, malignant hyperthermia is a rare but potentially life-threatening condition that requires prompt recognition and treatment to prevent serious complications and improve outcomes.

The condition is characterized by the excessive growth of gum tissue, which can lead to:

1. Redness and swelling of the gums
2. Bleeding while brushing or flossing
3. Bad breath (halitosis)
4. Pocket formation between the teeth and gums
5. Gum recession
6. Tooth loss

Gingival hyperplasia can be treated by addressing the underlying cause, improving oral hygiene, and undergoing scaling and root planing procedures to remove plaque and tartar. In severe cases, surgical intervention may be necessary to remove excess gum tissue and restore the natural contours of the mouth.

It is important for individuals to practice good oral hygiene, including brushing at least twice a day with fluoride toothpaste, flossing daily, and receiving regular dental cleanings to prevent gingival hyperplasia and other gum diseases. Early detection and treatment can help prevent the progression of the condition and restore the health of the teeth and gums.

Myocardial ischemia can be caused by a variety of factors, including coronary artery disease, high blood pressure, diabetes, and smoking. It can also be triggered by physical exertion or stress.

There are several types of myocardial ischemia, including:

1. Stable angina: This is the most common type of myocardial ischemia, and it is characterized by a predictable pattern of chest pain that occurs during physical activity or emotional stress.
2. Unstable angina: This is a more severe type of myocardial ischemia that can occur without any identifiable trigger, and can be accompanied by other symptoms such as shortness of breath or vomiting.
3. Acute coronary syndrome (ACS): This is a condition that includes both stable angina and unstable angina, and it is characterized by a sudden reduction in blood flow to the heart muscle.
4. Heart attack (myocardial infarction): This is a type of myocardial ischemia that occurs when the blood flow to the heart muscle is completely blocked, resulting in damage or death of the cardiac tissue.

Myocardial ischemia can be diagnosed through a variety of tests, including electrocardiograms (ECGs), stress tests, and imaging studies such as echocardiography or cardiac magnetic resonance imaging (MRI). Treatment options for myocardial ischemia include medications such as nitrates, beta blockers, and calcium channel blockers, as well as lifestyle changes such as quitting smoking, losing weight, and exercising regularly. In severe cases, surgical procedures such as coronary artery bypass grafting or angioplasty may be necessary.

There are several types of acidosis, including:

1. Respiratory acidosis: This occurs when the lung's ability to remove carbon dioxide from the blood is impaired, leading to an increase in blood acidity.
2. Metabolic acidosis: This type of acidosis occurs when there is an excessive production of acid in the body due to factors such as diabetes, starvation, or kidney disease.
3. Mixed acidosis: This type of acidosis is a combination of respiratory and metabolic acidosis.
4. Severe acute respiratory acidosis (SARA): This is a life-threatening condition that occurs suddenly, usually due to a severe lung injury or aspiration of a corrosive substance.

The symptoms of acidosis can vary depending on the type and severity of the condition. Common symptoms include:

1. Fatigue
2. Weakness
3. Confusion
4. Headaches
5. Nausea and vomiting
6. Abdominal pain
7. Difficulty breathing
8. Rapid heart rate
9. Muscle twitching

If left untreated, acidosis can lead to complications such as:

1. Kidney damage
2. Seizures
3. Coma
4. Heart arrhythmias
5. Respiratory failure

Treatment of acidosis depends on the underlying cause and the severity of the condition. Some common treatments include:

1. Oxygen therapy
2. Medications to help regulate breathing and heart rate
3. Fluid and electrolyte replacement
4. Dietary changes
5. Surgery, in severe cases.

In conclusion, acidosis is a serious medical condition that can have severe consequences if left untreated. It is important to seek medical attention immediately if you suspect that you or someone else may have acidosis. With prompt and appropriate treatment, it is possible to effectively manage the condition and prevent complications.

There are many different types of epilepsy, each with its own unique set of symptoms and characteristics. Some common forms of epilepsy include:

1. Generalized Epilepsy: This type of epilepsy affects both sides of the brain and can cause a range of seizure types, including absence seizures, tonic-clonic seizures, and atypical absence seizures.
2. Focal Epilepsy: This type of epilepsy affects only one part of the brain and can cause seizures that are localized to that area. There are several subtypes of focal epilepsy, including partial seizures with complex symptoms and simple partial seizures.
3. Tonic-Clonic Epilepsy: This type of epilepsy is also known as grand mal seizures and can cause a loss of consciousness, convulsions, and muscle stiffness.
4. Lennox-Gastaut Syndrome: This is a rare and severe form of epilepsy that typically develops in early childhood and can cause multiple types of seizures, including tonic, atonic, and myoclonic seizures.
5. Dravet Syndrome: This is a rare genetic form of epilepsy that typically develops in infancy and can cause severe, frequent seizures.
6. Rubinstein-Taybi Syndrome: This is a rare genetic disorder that can cause intellectual disability, developmental delays, and various types of seizures.
7. Other forms of epilepsy include Absence Epilepsy, Myoclonic Epilepsy, and Atonic Epilepsy.

The symptoms of epilepsy can vary widely depending on the type of seizure disorder and the individual affected. Some common symptoms of epilepsy include:

1. Seizures: This is the most obvious symptom of epilepsy and can range from mild to severe.
2. Loss of consciousness: Some people with epilepsy may experience a loss of consciousness during a seizure, while others may remain aware of their surroundings.
3. Confusion and disorientation: After a seizure, some people with epilepsy may feel confused and disoriented.
4. Memory loss: Seizures can cause short-term or long-term memory loss.
5. Fatigue: Epilepsy can cause extreme fatigue, both during and after a seizure.
6. Emotional changes: Some people with epilepsy may experience emotional changes, such as anxiety, depression, or mood swings.
7. Cognitive changes: Epilepsy can affect cognitive function, including attention, memory, and learning.
8. Sleep disturbances: Some people with epilepsy may experience sleep disturbances, such as insomnia or sleepiness.
9. Physical symptoms: Depending on the type of seizure, people with epilepsy may experience physical symptoms such as muscle weakness, numbness or tingling, and sensory changes.
10. Social isolation: Epilepsy can cause social isolation due to fear of having a seizure in public or stigma associated with the condition.

It's important to note that not everyone with epilepsy will experience all of these symptoms, and some people may have different symptoms depending on the type of seizure they experience. Additionally, some people with epilepsy may experience additional symptoms not listed here.

Symptoms of pheochromocytoma can include:

* Rapid heartbeat
* High blood pressure
* Sweating
* Weight loss
* Fatigue
* Headaches
* Nausea and vomiting

If left untreated, pheochromocytoma can lead to complications such as heart failure, stroke, and even death. Therefore, it is important that individuals who experience any of the above symptoms seek medical attention as soon as possible.

Treatment options for pheochromocytoma may include surgery to remove the tumor, medication to manage symptoms, and in some cases, radiation therapy. In rare cases, the tumor may recur after treatment, so regular monitoring is necessary to ensure that any new symptoms are detected early on.

Overall, while pheochromocytoma is a rare and potentially life-threatening condition, prompt medical attention and appropriate treatment can help manage symptoms and prevent complications.

A calcium channel is an ion channel which shows selective permeability to calcium ions. It is sometimes synonymous with voltage ... the receptor-operated calcium channels (in vasoconstriction) P2X receptors L-type calcium channel blockers are used to treat ... Calcium in biology - Use of calcium by organisms. "calcium channel" at Dorland's Medical Dictionary Striggow F, Ehrlich BE ( ... T-type calcium channel blockers are used to treat epilepsy. Increased calcium conductance in the neurons leads to increased ...
... s (CCB), calcium channel antagonists or calcium antagonists are a group of medications that disrupt the ... "Calcium-Channel Blockers (CCBs)". CV Pharmacology. Retrieved 2020-02-07. Domenic A. Sica, MD. "Calcium Channel Blocker-Related ... Ziconotide is a selective blocker of these calcium channels and acts as an analgesic. Calcium channel blockers came into wide ... Calcium Channel Antagonists". Poisoning & drug overdose (6th ed.). McGraw-Hill Medical. ISBN 978-0071668330. "calcium channel ...
A calcium channel opener is a type of drug which facilitates ion transmission through calcium channels. An example is Bay K8644 ... Calcium channel blocker Schramm M, Thomas G, Towart R, Franckowiak G (1983). "Activation of calcium channels by novel 1,4- ... Calcium permeable ion channels in lysosomal membranes that may be activated by a luminal pH increase include two pore channels ... This effect does most likely not occur by a direct interaction between the drug and a lysosomal calcium channel, but indirectly ...
The R-type calcium channel is a type of voltage-dependent calcium channel. Like the others of this class, the α1 subunit forms ... Ion channels, Electrophysiology, Integral membrane proteins, Calcium channels). ... "Entrez Gene: CACNA1E calcium channel, voltage-dependent, R type, alpha 1E subunit". Soong TW, Stea A, Hodson CD, Dubel SJ, ... This α1 subunit is also known as the calcium channel, voltage-dependent, R type, alpha 1E subunit (CACNA1E) or Cav2.3 which in ...
The Calcium-Dependent Chloride Channel (Ca-ClC) proteins (or calcium-activated chloride channels (CaCCs), are heterogeneous ... "1.A.17 The Calcium-Dependent Chloride Channel (Ca-ClC) Family". TCDB. Retrieved 16 April 2016. "Calcium activated chloride ... and calcium-dependent chloride channel anoctamin (ANO or TMEM16) channels ANO1 is highly expressed in human gastrointestinal ... possibly as Ca2+ channels or Ca2+ channel subunits (see also family TC# 1.A.82). Mice lacking both channels lack hair cell ...
... transient opening calcium channels) from the already well-known L-type calcium channels (Long-Lasting calcium channels). The ... Calcium channel blockers (CCB) such as mibefradil can also block L-type calcium channels, other enzymes, as well as other ... T-type calcium channels are low voltage activated calcium channels that become inactivated during cell membrane ... January 2016). "Anatomical localization of Cav3.1 calcium channels and electrophysiological effects of T-type calcium channel ...
N-type calcium channels also called Cav2.2 channels are voltage gated calcium channels that are localized primarily on the ... and this shows that only the N-type calcium channel, not the P/Q/L type calcium channels, are involved in the release of ... to block the N-type calcium channels, have produced alleviation of intractable pain. Blockade of the N-type calcium channel is ... blocking of N-type calcium channels reduce glomerular pressure through dilation of arterioles. N-type calcium channels have ...
... is the taking of too much of the medications known as calcium channel blockers (CCBs), either ... Calcium channel blockers, also known as calcium channel antagonists, are widely used for a number of health conditions. Thus ... The calcium channel blocker that caused the greatest number of deaths in 2010 in the United States was verapamil. This agent is ... Activated charcoal is recommended if it can be given within an hour or two of taking the calcium channel blockers. In those who ...
Calcium-activated potassium channels are potassium channels gated by calcium, or that are structurally or phylogenetically ... These channels can only be opened by increased levels of intracellular calcium. This trait of SK channels suggests that they ... BK channel SK channel Slow after-hyperpolarisation Vergara, C.; Latorre, R.; Marrion, N. V.; Adelman, J. P. (1998). "Calcium- ... Subtypes of IK Channels KCa3.1 (IKCa1, SK4, KCNN4) Small conductance calcium activate potassium channels are quite different ...
Calcium channel blocker (including section on non-dihydropyridine calcium channel blockers) Calcium channel Dihydropyridine ... Dihydropyridine calcium channel blockers are derivatives of 1,4-dihydropyridine that are used as L-type calcium channel ... Compared with certain other L-type calcium channel blockers (for example those of the phenylalkylamine class such as verapamil ... Dihydropyridine class L-type calcium channel blockers include, in alphabetical order (brand names vary in different countries ...
L-type calcium channels were peptide sequenced and it was found that there were 4 kinds of L-type calcium channels: α1S ( ... The L-type calcium channel (also known as the dihydropyridine channel, or DHP channel) is part of the high-voltage activated ... calcium-induced-calcium-release). Phosphorylation of these channels increases their permeability to calcium and increases the ... Unlike other voltage gated calcium channels, L-type calcium channels are resistant to ⍵-CT X (GVIA) and ⍵-AG A (IVA) inhibitory ...
... opening of the L-type calcium channel permits influx of calcium into the cell. The calcium binds to the calcium release ... High-voltage-gated calcium channels include the neural N-type channel blocked by ω-conotoxin GVIA, the R-type channel (R stands ... Voltage-gated calcium channels (VGCCs), also known as voltage-dependent calcium channels (VDCCs), are a group of voltage-gated ... In skeletal muscle, the actual opening of the channel, which is mechanically gated to a calcium-release channel (a.k.a. ...
Calcium release-activated channels (CRAC) are specialized plasma membrane Ca2+ ion channels. When calcium ions (Ca2+) are ... Hou X, Pedi L, Diver MM, Long SB (December 2012). "Crystal structure of the calcium release-activated calcium channel Orai". ... forms the pore of the CRAC channel. The protein ORAI1 is a structural component of the CRAC calcium channel. ORAI1 interacts ... Zhou Y, Ramachandran S, Oh-Hora M, Rao A, Hogan PG (March 2010). "Pore architecture of the ORAI1 store-operated calcium channel ...
The Q-type calcium channel is a type of voltage-dependent calcium channel. Like the others of this class, the α1 subunit is the ... Ion channels, Electrophysiology, Membrane biology, Integral membrane proteins, Calcium channels). ... Q-Type+Calcium+Channel at the US National Library of Medicine Medical Subject Headings (MeSH) (Articles with short description ... They are poorly understood, but like R-type calcium channels, they appear to be present in cerebellar granule cells. They have ...
The P-type calcium channel is a type of voltage-dependent calcium channel. Similar to many other high-voltage-gated calcium ... type calcium channels are voltage-dependent calcium channels that are classified under the high voltage activated class channel ... P-type calcium channel blockers act to impede the flow of calcium. The blocking of calcium currents may cause the organism to ... P-type calcium channels play a similar role to the N-type calcium channel in neurotransmitter release at the presynaptic ...
... (CCAT) is a transcription factor found in mammalian cells. In neuronal ... "A Promoter in the Coding Region of the Calcium Channel Gene CACNA1C Generates the Transcription Factor CCAT". PLOS ONE. 8 (4): ... the gene that encodes the voltage-gated calcium channel Cav1.2. Gomez-Ospina, Natalia; Panagiotakos, Georgia; Portmann, Thomas ...
"IP3-sensitive calcium channel". In Lee, A. G. (ed.). Transmembrane Receptors and Channels. Transmembrane Receptors and Channels ... The channel domains possess six putative TMSs and a putative channel lining region between TMSs 5 and 6. Both the large N- ... Channels are activated by IP3 binding, and like the Ry receptors, the activities of the IP3 receptor channels are regulated by ... Santulli, Gaetano; Marks, Andrew (2015). "Essential Roles of Intracellular Calcium Release Channels in Muscle, Brain, ...
Voltage sensing in thermo-TRP channels has been reviewed by Brauchi et al. TRP channels have six TMS helices. These channels ... 2F37​ Transient receptor potential cation channel subfamily A member 1: PDB: 3J9P​ Voltage-gated ion channel Ion channel ... The transient receptor potential Ca2+ channel (TRP-CC) family (TC# 1.A.4) is a member of the voltage-gated ion channel (VIC) ... which regulates calcium uptake and homeostasis. It is essential for channel assembly and regulation. The 1.7 Å crystal ...
... increases the calcium sensitivity of the BK channel. It does this by enhancing the time spent by the channel in burst-like open ... the calcium-activated potassium channel beta subunit is a family of proteins comprising the beta subunits of calcium-activated ... "Functional role of the beta subunit of high conductance calcium-activated potassium channels". Neuron. 14 (3): 645-50. doi: ... The functional diversity of potassium channels can arise through homo- or hetero-associations of alpha subunits or association ...
... also known as large conductance calcium-activated potassium channel, ... BK channel Calcium-activated potassium channel Voltage-gated potassium channel GRCh38: Ensembl release 89: ENSG00000156113 - ... and calcium-dependent K+ channel, a distinct member of voltage-dependent ion channels with seven N-terminal transmembrane ... Structure of the intracellular gating ring from the human high-conductance Ca2+ gated K+ channel (BK Channel) BK channels are ...
... a protein in the voltage-dependent calcium channel complex. Calcium channels mediate the influx of calcium ions into the cell ... Calcium channel, voltage-dependent, T type, alpha 1H subunit, also known as CACNA1H, is a protein which in humans is encoded by ... "Entrez Gene: CACNA1H calcium channel, voltage-dependent, T type, alpha 1H subunit". Cribbs LL, Lee JH, Yang J, Satin J, Zhang Y ... 2003). "T-type calcium channel regulation by specific G-protein betagamma subunits". Nature. 424 (6945): 209-13. doi:10.1038/ ...
The calcium channels are used for cell signaling and triggering apoptosis. The calcium uniporter transports calcium across the ... Hoppe, U. (2010). "Mitochondrial Calcium Channels". FEBS Letters: 1975-1981. OpenStax College (2013). Chapter 12.4 The Action ... Uniporter channels open in response to a stimulus and allow the free flow of specific molecules. There are several ways in ... Voltage-gated potassium channels are also uniporters that can be found in neurons and are essential for action potentials. This ...
... cell biology and biochemistry of store-operated calcium channel proteins. Opening of these channels leads to calcium entry into ... Too much or too little calcium entry can lead to disease and tissue damage which makes the Calcium release activated channels ( ... Parekh's research investigates the physiology of Calcium signalling and Calcium release activated channels (CRACs). He ... Anant Parekh's ORCID 0000-0002-4860-1644 Parekh, Anant B.; Putney, James W. (2005). "Store-Operated Calcium Channels". ...
"Calcium channel characteristics conferred on the sodium channel by single mutations". Nature. 356 (6368): 441-443. Bibcode: ... Namely, Na + {\displaystyle {\text{Na}}^{+}} ions in a pure sodium solution pass unimpeded through a calcium channel, but are ... In selective ion channels, the favoured ionic species passes through the channel almost at the rate of free diffusion, despite ... Krauss, Daniel; Eisenberg, Bob; Gillespie, Dirk (2011-03-06). "Selectivity sequences in a model calcium channel: role of ...
... sensor protein responsible for sensing calcium changes in internal calcium stores and communicate with ORAI calcium channels in ... STIM-ORAI Interactions That Control the CRAC Channel. Current Topics in Membranes. Store-Operated Calcium Channels. Vol. 71. ... "STIM1 gates the store-operated calcium channel ORAI1 in vitro". Nature Structural & Molecular Biology. 17 (1): 112-116. doi: ... Hogan, Patrick G.; Lewis, Richard S.; Rao, Anjana (2010-01-01). "Molecular Basis of Calcium Signaling in Lymphocytes: STIM and ...
This gene encodes an alpha-1 subunit of a voltage-dependent calcium channel. Calcium channels mediate the influx of calcium ... Calcium channel Calcium channel associated transcriptional regulator ENSG00000285479 GRCh38: Ensembl release 89: ... When calcium ions bind to calmodulin, which in turn binds to a Cav1.2 channel, it allows the Cav1.2 channels within a cluster ... The calcium channel consists of a complex of alpha-1, alpha-2/delta and beta subunits in a 1:1:1 ratio. The S3-S4 linkers of ...
However, other ions such as calcium may be important and there is a great diversity of channels for all ions. As an example, ... and IL are currents conveyed through the local sodium channels, potassium channels, and "leakage" channels (a catch-all), ... Yamada WM, Koch C, Adams PR (1989). "Multiple Channels and Calcium Dynamics". In C. Koch, I Segev (ed.). Methods in Neuronal ... can be generated on membranes with voltage-sensitive calcium channels and different types of sodium/potassium channels. The ...
It acts as an N-type voltage-gated calcium channel (Cav2.2) blocker and is highly selective for this channel over the related P ... 225-. ISBN 978-1-84973-645-9. Stephens G, Mochida S (23 April 2013). Modulation of Presynaptic Calcium Channels. Springer ... type voltage-gated calcium channel (Cav2.1). Relative to ziconotide, leconotide is advantageous in that it is significantly ... Calcium channel blockers, Peptides, All stub articles, Analgesic stubs). ...
venom that block calcium ion channels". Toxicon. 52 (2): 228-236. doi:10.1016/j.toxicon.2008.05.019. PMID 18606178. Biolib ...
It blocks two potassium channel subtypes; voltage-gated and calcium-activated channels. Coba is a region in Mexico where the ... Other voltage-dependent K+-channels that are blocked by Cobatoxin 1 are the Kv1.2 K+-channels in rats and Kv1.3 K+-channels in ... Cobatoxin 1 and 2 both block the Kv1.1 K+-channels in mice and the Shaker B K+ channels in insects, which are voltage-dependent ... The α-KTx family is part of the K+-channel-specific scorpion toxins (KTx), which consists of 3 families; α, β, and γ. These 3 ...
For example, muscle contraction depends upon the movement of calcium, sodium and potassium through ion channels in the cell ... About 99% of a human's body weight is made up of the elements carbon, nitrogen, calcium, sodium, chlorine, potassium, hydrogen ... The most important ions are sodium, potassium, calcium, magnesium, chloride, phosphate and the organic ion bicarbonate. The ... Electrolytes enter and leave cells through proteins in the cell membrane called ion channels. ...
The production of bone char was featured on the Discovery Channel's TV series Dirty Jobs, on episode 24 of season 4, "Bone ... calcium carbonate 6-10% and carbon 7-10%. It is primarily used for filtration and decolorisation. Bone char is primarily made ... most importantly sulfates and the ions of magnesium and calcium. The removal of these is beneficial, as it reduces the level of ...
The most widely used tocolytics include beta agonists, calcium channel blockers, and magnesium sulfate. The goal of ... three channels to pass through it: the urethra, the vagina and the rectum. The infant's head and shoulders must go through a ...
It later becomes incorporated into the CatSper complex, a specialized calcium ion channel that enables spermatozoa motility. ... Liu J, Xia J, Cho KH, Clapham DE, Ren D (June 2007). "CatSperbeta, a novel transmembrane protein in the CatSper channel complex ... Liu J, Xia J, Cho KH, Clapham DE, Ren D (June 2007). "CatSperbeta, a novel transmembrane protein in the CatSper channel complex ...
... it is rich in calcium, protein, and iron, among other nutrients, and could potentially fight altitude sickness- a popular ... expressed support for greater legal channels for migration, and stated that all migrants, regardless of their legal status, ...
Calcium channel, voltage-dependent, L type, alpha 1C subunit), DPYD (Dihydropyrimidine dehydrogenase [NADP+]), CACNB2 (Voltage- ... dependent L-type calcium channel subunit beta-2), TSSK6 (Testis-Specific Serine Kinase 6), NT5DC2 (Cytosolic 5'-nucleotidase), ...
Mn2+ enters through voltage dependent calcium channels, is taken into intracellular organelles and is transported by the ...
... polycystin cation channels, glutamate-gated ion channels, calcium-dependent chloride channels, monovalent cation:proton ... Voltage-gated sodium channels and calcium channels are made up of a single polypeptide with four homologous domains. Each ... Voltage-gated ion-channels are usually ion-specific, and channels specific to sodium (Na+), potassium (K+), calcium (Ca2+), and ... With sixteen different identified genes for human calcium channels, this type of channel differs in function between cell types ...
Calcium Channel Blockers: Help slow the heart rate by blocking the number of electrical impulses that pass through the AV node ... 35 Adenosine Beta-blocker Calcium channel antagonist Digoxin Excitation (vagal stimulation) LAMB:p. 35 Lidocaine Amiodarone ...
After Soviet science was liberalized in the 1960s, he moved to ion channels, developing as a leader in the actions of local ... Duchen at the University College London, Khodorov was studying calcium homeostasis, glutamate excitotoxicity and mitochondrial ... At the Vishnevsky Institute of Surgery, the Khodorov laboratory carried out pioneering studies in the field of ion channel ... Sobolevsky, Alexander I.; Koshelev, Sergey G.; Khodorov, Boris I. (December 1999). "Probing of NMDA Channels with Fast Blockers ...
... there is a short-circuit channel (i.e. a highly K-permeable ion channel) for potassium in the membrane, thus the voltage across ... This increased presence of calcium is what allows for the force of contraction to be increased. In the case of patients where ... Blaustein MP (May 1977). "Sodium ions, calcium ions, blood pressure regulation, and hypertension: a reassessment and a ... begin to increase within the cell which ultimately increases the concentration of intracellular calcium via the sodium-calcium ...
Ions of elements like calcium and sulphur dissolve easily when the permafrost thaws. List of longest rivers of Canada List of ... This means that a channel can be followed for a longer distance downriver until it, itself, disseminates into the shared delta ... However, a distributary of the Peel is the headwater for a channel that later collects distributaries of the Mackenzie. ...
Other research has also suggested that calcium flow through N-type calcium channels is essential for normal breathing, and is ... Other potassium channels like large conductance calcium-dependent potassium channels and sodium chloride dependent potassium ... voltage gated calcium channels become activated and calcium is able to flow into the cell which usually leads to the release of ... L-type calcium channels are known to increase the frequency of action potentials in some neurons, which might be the reason ...
In addition, calcium hydroxide commonly being produced by calcination of calcium carbonate releases yet more carbon dioxide ... According to a Discovery Channel article on Sonic Sea Journeys Deep into the Ocean over the last century, extremely loud noise ... usually calcium sulfate if flue gases are scrubbed by being passed through calcium hydroxide solution) which would have to be ...
... calcium channel blockers, and phenytoin) HHS is usually precipitated by an infection, myocardial infarction, stroke or another ...
Calcium release from IP3 sensitive calcium stores activates calcium dependent chloride channels. These chloride channels ... The specific mechanism for the contraction of smooth muscle in the GI tract depends upon IP3R calcium release channels in the ... Longitudinal muscle fibers depend on calcium influx into the cell for excitation-contraction coupling, while circular muscle ... or by receptor mediated calcium influx. These efferent motor neurons of the enteric nervous system are cholinergic and ...
... the CNG ion channel is open allowing sodium and calcium to rush into the cell. The influx of calcium begins a cascade of events ... Calcium first binds to calmodulin to form CaM. CaM will then bind to the CNG channel and close it, stopping the sodium and ... opens ion channels in the cell membrane, resulting in an influx of sodium and calcium ions into the cell, and an efflux of ... Touhara, Kazushige (2009). "Insect Olfactory Receptor Complex Functions as a Ligand-gated Ionotropic Channel". Annals of the ...
Fox News Channel reporter, previously a CNN reporter and host of The New Music on MuchMusic Lloyd Robertson OC LLD (hc) (born ... invented arc lamps and process for creating calcium carbide Henry Woodward - co-inventor of the first electric light bulb ...
One calculation by Y. Gambhir et al., analyzing nuclear binding energy and stability in various decay channels, suggests a ... was first attempted in 1985 by bombarding a target of einsteinium-254 with calcium-48 ions at the superHILAC accelerator at ...
... the β and γ subunits interact with N-type voltage gated calcium channels, to reduce action potential mediated influx of calcium ... Silver RB, Poonwasi KS, Seyedi N, Wilson SJ, Lovenberg TW, Levi R (Jan 2002). "Decreased intracellular calcium mediates the ... "Histamine Receptors: H3". IUPHAR Database of Receptors and Ion Channels. International Union of Basic and Clinical Pharmacology ...
"Maldini shirt waits for 3G". Channel 4. 26 May 2007. Archived from the original on 27 May 2007. Retrieved 26 May 2007. Rogers, ... "Sassuolo retire legendary Francesco Magnanelli jersey #4". U.S. Sassuolo Calcio. 5 July 2022. Retrieved 5 July 2022. "Ненад ...
The σ1 receptor has been shown to appear in a complex with voltage gated K+ channels (Kv1.4 and Kv1.5), leading to the idea ... that modulates calcium signaling through the IP3 receptor. In humans, the σ1 receptor is encoded by the SIGMAR1 gene. The σ1 ... Zhang H, Cuevas J (June 2005). "sigma Receptor activation blocks potassium channels and depresses neuroexcitability in rat ... and inhibition of voltage gated K+ channels. The reasons for these effects are not well understood, even though σ1 receptors ...
Subjects covered in the book include both traditional approaches to looking at arrhythmia, such as ion channel effects, and ... Novel ideas offered included studying sodium-calcium exchanger and ryanodine receptor effects. One chapter (5) is dedicated to ...
Charpentier investigates what produces calcium oscillations and how calcium channels affect plant development and has published ... "Nuclear-localized cyclic nucleotide-gated channels mediate symbiotic calcium oscillations". Science. 352 (6289): 1102-1105. ... Nuclear calcium machinery is common to all land plants, her laboratory is exploring how this has evolved and functions across ... Her team showed that calcium can be released by the nucleus of root apical meristem - the region of the growing root. Using ...
Gillman has been featured in several media outlets, news channels, and such as BBC, and academic journals like Lancet, BMJ, ... Gillman, Mark A. (1 October 1991). "Calcium Hydroxide and Sporadic Clinical Mycotoxicosis". Nutrition and Health. 7 (4): 199- ...
... closing calcium channels, and opening potassium channels. Opioids like oxycodone are thought to produce their analgesic effects ...
"Outcomes of Unintentional beta-Blocker or Calcium Channel Blocker Overdoses: a Retrospective Review of Poison Center Data" (PDF ... and discussed the outcomes of unintentional beta-blocker or calcium channel blocker overdoses among patients. Furthermore, he ...
Some observations show that Mercury is surrounded by a hot corona of calcium atoms with temperature between 12,000 and 20,000 K ... During its 2009 flyby, the Ultraviolet and Visible Spectrometer (UVVS) channel of the Mercury Atmospheric and Surface ... Observations by the MESSENGER probe in 2009 showed that calcium is concentrated mainly near the equator-opposite to what is ... In 1998 another element, calcium (Ca), was detected with column density three orders of magnitude below that of sodium. ...
Its black, wrinkled petioles are 0.7-1.6 centimeters with a channel on their upper surfaces. It leathery, hairless, oblong to ... It has been observed growing in lowland forests with soil rich in calcium carbonate at elevations of 60 to 300 meters. ...
Calcium channel blockers prevent calcium from entering the muscle cells of your heart and blood vessels. This allows the blood ... Calcium Channel Blockers (Mayo Foundation for Medical Education and Research) Also in Spanish ... Calcium Supplements: Do They Interfere with Blood Pressure Drugs? (Mayo Foundation for Medical Education and Research) Also in ...
Populations of channels in single spines are depressed stochastically and synchronously, independent of channels in the parent ... constitute a major source of calcium ions in dendritic spines, but their function is unknown. Here we show that R-type VSCCs in ... Budde, T., Meuth, S. & Pape, H.C. Calcium-dependent inactivation of neuronal calcium channels. Nat. Rev. Neurosci. 3, 873-883 ( ... Brehm, P. & Eckert, R. Calcium entry leads to inactivation of calcium channel in Paramecium. Science 202, 1203-1206 (1978). ...
Through spatial and temporal control of intracellular calcium concentration, voltage-sensitive calcium channels regulate a host ... This article reviews the structural and functional diversity of neuronal calcium channels and the therapeutic potential of ... Through spatial and temporal control of intracellular calcium concentration, voltage-sensitive calcium channels regulate a host ... Antagonists of neuronal calcium channels: structure, function, and therapeutic implications Annu Rev Pharmacol Toxicol. 1995;35 ...
SEARCH RESULTS for: Calcium Channel Antagonists [Drug Class] (837 results) *Share : JavaScript needed for Sharing tools. ...
Calcium Channel Blockers are often considered as a potential cause of developing edema. ... Muscle cells require calcium to contract, so the main purpose of calcium channel blockers is to make it difficult for the ... According to Mayo Clinic, calcium channel blockers are medications that prevent calcium from entering into the muscle cells in ... Calcium channel blockers, come in many forms, including short-acting medications and long-acting medications. Verapamil, ...
Calcium channel blockers. Class Summary. These drugs are used for rate control in atrial fibrillation or another SVT. They ... Tachydysrhythmias may be treated with calcium channel blockers or beta-blockers (preferred) for rate control or with ... Before administration, control ventricular rate with another agent (eg, calcium channel blocker). Drug of choice for life- ... Decreases conduction velocity in AV node and increases refractory period by blocking calcium influx, converting SVT or slowing ...
Protein target information for Voltage-dependent calcium channel gamma-2 subunit (dog). Find diseases associated with this ...
Store-operated calcium channels Anant B Parekh et al. Physiol Rev. 2005 Apr. ... Store-operated calcium channels Anant B Parekh 1 , James W Putney Jr ... Neuronal Store-Operated Calcium Channels. Bouron A. Bouron A. Mol Neurobiol. 2023 Aug;60(8):4517-4546. doi: 10.1007/s12035-023- ... Store-operated calcium entry: a tough nut to CRAC. Penner R, Fleig A. Penner R, et al. Sci STKE. 2004 Jul 20;2004(243):pe38. ...
Inositol 1,4,5-trisphosphate (IP3) receptors are a form of ligand-gated ion channels that are activated by cytosolic Ca2+ and ... Inositol 1,4,5-trisphosphate (IP3) receptors are a form of ligand-gated ion channels that are activated by cytosolic Ca2+ and ...
Antibodies for proteins involved in calcium channel regulator activity pathways, according to their Panther/Gene Ontology ...
Calcium Channel Blockers. Nicardipine (Cardene, Cardene IV, Cardene SR). *View full drug information ...
Calcium Channels and Local and Long Distance Signaling on Both Sides of the Synapse ... Their work is centered around biophysical analysis of the behavior of individual channel molecules, using single-channel and ... Their work is centered around biophysical analysis of the behavior of individual channel molecules, using single-channel and ... Ion channels are the elementary excitable elements in the cell membranes of nerve, muscle, and many other cells where they ...
Calcium channel blockers as antihypertensive agents : a need for caution : reports on individual drugs  ...
Because muscle contraction is largely dependent upon influx of calcium, its inhibition causes relaxation, particularly in ... The calcium channel blockers act by blocking the influx of calcium ions into vascular smooth muscle and cardiac muscle cells ... calcium channel blockers. Several of the calcium channel blockers are now available in generic forms and some are available as ... The calcium channel blockers act by blocking the influx of calcium ions into vascular smooth muscle and cardiac muscle cells ...
PILOT STUDY OF A CALCIUM CHANNEL BLOCKER IN FEMALES WITH BIPOLARDISORDER NIH Guide, Volume 25, Number 20, June 21, 1996 RFP ... "Pilot Study of a Calcium Channel Blocker in Females with Bipolar Disorder" to (1) determine in the most cost effective manner, ... preliminary evidence of efficacy for calcium channel blockers such as verapamil in bipolar disorder, and (2) recruit ...
... by the P/Q-type calcium channel blocker agatoxin IVB, suggesting that P/Q-type calcium channels are the major targets involved ... Inhibition of calcium channels. GABAB receptors reduced Ca2+currents in SCN neurons. The channel that showed the greatest ... Reduction of baclofen inhibition after blocking P/Q-type calcium channels. A, Comparison of baclofen inhibition of calcium ... P/Q-type calcium channels are the major target of GABABreceptor modulation. Whole-cell Ca2+ currents, using Ba2+ as the carrier ...
administration of a calcium channel blocker, now estimated to be part of the treatment of 25% of hypertensive patients, can ... 1985) Therapeutic effect of calcium channel blockade in primary aldosteronism. J Clin Endocrinol Metab 60:896-899. ... 1986) Participation of voltage-dependent calcium channels in the regulation of adrenal glomerulosa function by angiotensin II ... calcium blockade. Since its first recognition, the prevalence of primary hyperaldosteronism, or Conns syndrome, as a cause of ...
1984) Non-selective conductance in calcium channels of frog muscle: calcium selectivity in a single-file pore The Journal of ... 1992) Calcium channel characteristics conferred on the sodium channel by single mutations Nature 356:441-443. ... 2015) Calcium binding proteins and calcium signaling in prokaryotes Cell Calcium 57:151-165. ... These new channels will also help to understand the evolution of the mechanisms of calcium-selectivity in all Ca2+-permeable ...
Extracellular pH modulates block of both sodium and calcium channels by nicardipine. ... Extracellular pH modulates block of both sodium and calcium channels by nicardipine. Journal Article (Journal Article) ... In contrast the Ca channel has been reported not to show such an effect. Because of the absence of this response, a two-site ... For ICa, tau r also increased from 1.43 +/- 0.55 to 2 +/- 0.32 s. For each channel type, the results are well explained by a ...
Calcium-activated chloride channel A4 (CLCA4) is known as a tumor suppressor which contributes to the progression of a number ... BACKGROUND: Calcium-activated chloride channel A4 (CLCA4) is known as a tumor suppressor which contributes to the progression ... Calcium-Activated Chloride Channel A4 (CLCA4) Plays Inhibitory Roles in Invasion and Migration Through Suppressing Epithelial- ... Keywords: Cell Migration Inhibition, Colorectal Neoplasms, Epithelial-mesenchymal transition, Neoplasm Invasiveness, Calcium, ...
Antidiarrheal and antispasmodic activities of Vincetoxicum stocksii are mediated through calcium channel blockade Download ...
Calcium channel blocker maintenance therapy is one of the types of tocolytic therapy that may be used after an episode of ... Maintenance therapy with calcium channel blockers for preventing preterm birth after threatened preterm labour. Overview of ... Maintenance therapy with calcium channel blockers for preventing preterm birth after threatened preterm labour ...
Maitotoxin: effects on calcium channels, phosphoinositide breakdown, and arachidonate release in pheochromocytoma PC12 cells.. ... Maitotoxin: effects on calcium channels, phosphoinositide breakdown, and arachidonate release in pheochromocytoma PC12 cells.. ... Maitotoxin: effects on calcium channels, phosphoinositide breakdown, and arachidonate release in pheochromocytoma PC12 cells.. ... Maitotoxin: effects on calcium channels, phosphoinositide breakdown, and arachidonate release in pheochromocytoma PC12 cells. ...
Molecular determinants of drug binding ad action on L-type calcium channels. In: Annual Review of Pharmacology and Toxicology. ... Molecular determinants of drug binding ad action on L-type calcium channels. / Hockerman, Gregory H.; Peterson, Blaise; Johnson ... Molecular determinants of drug binding ad action on L-type calcium channels. Annual Review of Pharmacology and Toxicology. 1997 ... Dive into the research topics of Molecular determinants of drug binding ad action on L-type calcium channels. Together they ...
R Type Calcium Channels; R Type Calcium Channel; Channel, R-. Type Calcium; Calcium Channels, R Type; Calcium Channel, R-. Type ... Dependent Calcium Channels; R-. Type VDCC; R-. Type Calcium Channel; R-. Type Calcium Channels ... Calcium Channels, R-Type *Cation Transport Proteins. Cacna1e protein, mouse 0 *Calcium Channels, R-Type *Cation Transport ... Calcium Channels, R-Type *Cation Transport Proteins. J Biol Chem 1994 Sep 2;269(35):22347-57 To share this definition, click " ...
Other categories referring to Low threshold calcium spikes were antagonized by T-channel blockers in rat ... Low threshold calcium spikes were antagonized by T-channel blockers in rat ...
Downloading a figure as powerpoint requires a browser with javascript support. Enable javascript and try again For help please contact [email protected] ...
voltage-gated calcium channel activity of Voltage-gated Calcium Channels (pancreatic beta cell) [plasma membrane] ...
Role of Voltage-Gated Calcium Channels in Hearing. *Robertson, Donald (Chief Investigator) ...
Neurons express multiple types of voltage-gated calcium (Ca2+) channels. Two subtypes of neuronal L-type Ca2+ channels are ... N2 - Neurons express multiple types of voltage-gated calcium (Ca2+) channels. Two subtypes of neuronal L-type Ca2+ channels are ... AB - Neurons express multiple types of voltage-gated calcium (Ca2+) channels. Two subtypes of neuronal L-type Ca2+ channels are ... "Association of Cav1.3 L-type calcium channels with shank",. abstract = "Neurons express multiple types of voltage-gated calcium ...
  • Ingestion of excessive calcium channel blockers (CCBs) is one of the most potentially lethal prescription drug overdoses. (medscape.com)
  • Calcium Channel Blockers are often considered as a potential cause of developing edema. (progressivehealth.com)
  • Healthcare experts around the world prescribe calcium channel blockers to treat several health conditions, including migraine headaches, high blood pressure , circulatory issues, and complications of brain aneurysms. (progressivehealth.com)
  • Calcium channel blockers, come in many forms, including short-acting medications and long-acting medications. (progressivehealth.com)
  • Verapamil, diltiazem, and nifedipine are among the calcium channel blockers listed by MedlinePlus. (progressivehealth.com)
  • The common side effects of calcium channel blockers include peripheral edema or swelling of the legs , feet, and ankles from the accumulation of fluid. (progressivehealth.com)
  • According to Mayo Clinic, calcium channel blockers are medications that prevent calcium from entering into the muscle cells in the heart and around the blood vessels. (progressivehealth.com)
  • Muscle cells require calcium to contract, so the main purpose of calcium channel blockers is to make it difficult for the muscle cells in the heart and blood vessels to contract. (progressivehealth.com)
  • According to a study published in the 'Journal of Clinical Hypertension' in 2003, calcium channel blockers may cause edema due to their effects on the blood pressure in different blood vessels. (progressivehealth.com)
  • The most effective way of treating edema associated with calcium channel blockers is to change the medication being used. (progressivehealth.com)
  • As per the Journal of Clinical Hypertension, some calcium channel blockers are less likely to cause peripheral edema . (progressivehealth.com)
  • Tachydysrhythmias may be treated with calcium channel blockers or beta-blockers (preferred) for rate control or with antidysrhythmics, depending on the rhythm disturbance. (medscape.com)
  • Calcium-channel blockers are a type of medicine used to treat high blood pressure and heart rhythm disturbances. (medlineplus.gov)
  • Other medicines may also contain calcium-channel blockers. (medlineplus.gov)
  • Calcium channel blockers : a need for reassessment? (who.int)
  • The calcium channel blockers act by blocking the influx of calcium ions into vascular smooth muscle and cardiac muscle cells during membrane depolarization. (nih.gov)
  • Thus, the major effects of the calcium channel blockers are relaxation of vascular and arterial smooth muscle cells resulting in arterial vasodilation. (nih.gov)
  • The major use of the calcium channel blockers is for hypertension and angina pectoris (variant, exertional, and unstable). (nih.gov)
  • Some calcium channel blockers are also used for supraventricular arrhythmias and heart failure. (nih.gov)
  • These agents are also commonly referred to as being first generation (verapamil, diltiazem, nifedipine) or second generation (amlopine, felodipine, isradipine, nicardipine, nimodipine and others) calcium channel blockers. (nih.gov)
  • Among the different classes of antihypertensive drugs, calcium channel blockers (CCBs) are widely used for the management of hypertension. (psychreg.org)
  • Calcium-channel blockers or calcium antagonist have several possible modes of action in hypertension. (nursinganswers.net)
  • Because calcium-channel blockers inhibit renin release, the renin-angiotensin system may also be suppressed. (nursinganswers.net)
  • Calcium-channel blockers prove to be useful in hypertensive patients who also have stable angina and spastic angina (Brunton, Chabner, & Knollman, 2011). (nursinganswers.net)
  • The vasodilation properties of calcium-channel blockers lead to a reduction in after-load, and their regional smooth muscle relaxant properties are useful in relieving coronary spasms. (nursinganswers.net)
  • Calcium-channel blockers are also useful in treating patients who cannot take beta-blocking agents (Katzung, Mastes, & Trevor, 2012). (nursinganswers.net)
  • Calcium channel blockers are medicines that relax the muscles that make up the walls of your arteries. (www.nhs.uk)
  • Grapefruit juice interacts with some calcium channel blockers and increases the level of the medicine in your blood. (www.nhs.uk)
  • Effect of dihydropyridine calcium channel blockers on blood pressure variability in the SPRINT trial: a treatment effects approach. (nih.gov)
  • Prior research has suggested that dihydropyridine calcium channel blockers (CCB) may reduce vvBPV, which we attempted to verify in a high-quality dataset with robust statistical methodology. (nih.gov)
  • The image below illustrates the chemical structure of the calcium channel blocker diltiazem. (medscape.com)
  • Before administration, control ventricular rate with another agent (eg, calcium channel blocker). (medscape.com)
  • Calcium-channel blocker overdose occurs when someone takes more than the normal or recommended amount of this medicine. (medlineplus.gov)
  • The specific ingredients in each type of calcium-channel blocker vary. (medlineplus.gov)
  • Taking too much of a calcium-channel blocker can be very dangerous. (medlineplus.gov)
  • Verapamil (a type of calcium channel blocker) overdose is associated with the highest mortality risk. (medlineplus.gov)
  • This learning resource is a 5-minute animation about calcium channel blocker in YouTube. (merlot.org)
  • In fact, there is no need for too much investigation can aspirin help to lower blood pressure As early as the beginning of the earthquake, the US troops stationed in the cities along the Sea of Japan calcium channel blocker blood pressure pills. (leduel.com)
  • At the end of the game, the Real Madrid players hugged each other, looking very excited This feeling is not much how much will Ativan lower blood pressure different from that at the end of the calcium channel blocker blood pressure pills Champions League final. (leduel.com)
  • But I didn't want Zhang Xiaolong to say calcium channel blocker blood pressure pills lightly We are here only to save people, not to fight fiercely. (leduel.com)
  • However, the main ingredient is called a calcium-channel antagonist. (medlineplus.gov)
  • Decreases conduction velocity in AV node and increases refractory period by blocking calcium influx, converting SVT or slowing rate in atrial fibrillation. (medscape.com)
  • Because muscle contraction is largely dependent upon influx of calcium, its inhibition causes relaxation, particularly in arterial beds. (nih.gov)
  • However, we have recently found that under hyperpolarized conditions, the T-type calcium channel can trigger a large after-depolarization and a corresponding influx of calcium into dopamine neuron dendrites. (nih.gov)
  • Lercanidipine is a third-generation dihydropyridine CCB that selectively blocks L-type calcium channels in vascular smooth muscle cells. (psychreg.org)
  • Calcium-activated chloride channel A4 (CLCA4) is known as a tumor suppressor which contributes to the progression of a number of types of malignant tumors. (medscimonit.com)
  • Calcium-activated chloride channel ANO1 promotes breast cancer progression by activating EGFR and CAMK signaling. (nih.gov)
  • The calcium-activated chloride channel anoctamin 1 (ANO1) is located within the 11q13 amplicon, one of the most frequently amplified chromosomal regions in human cancer, but its functional role in tumorigenesis has remained unclear. (nih.gov)
  • Moreover, ANO1 chloride channel activity was important for cell viability. (nih.gov)
  • Mechanistically, ANO1 knockdown or pharmacological inhibition of its chloride-channel activity reduced EGF receptor (EGFR) and calmodulin-dependent protein kinase II (CAMKII) signaling, which subsequently attenuated AKT, v-src sarcoma viral oncogene homolog (SRC), and extracellular signal-regulated kinase (ERK) activation in vitro and in vivo. (nih.gov)
  • Our results highlight the involvement of the ANO1 chloride channel in tumor progression and provide insights into oncogenic signaling in human cancers with 11q13 amplification, thereby establishing ANO1 as a promising target for therapy in these highly prevalent tumor types. (nih.gov)
  • Overall, we have indentified an unrecognized regulation pathway of T-type calcium channels by SNARE proteins, and proposed the first molecular mechanism by which T-type channels could mediate low-threshold exocytosis. (inserm.fr)
  • The CRAC channels are composed of three plasma membrane based proteins, known as Orai1, Orai2 and Orai3 and two Ca2+ sensor proteins STIM1 and STIM2 in the endoplasmic reticulum. (cmos.org.tr)
  • Another system regulated by intracellular calcium is the release of renin by the cells of the kidney. (nursinganswers.net)
  • Synergistic activation by membrane voltage and intracellular Ca2+ is a unique property of large conductance Ca2+ activated K+ (BK) channels, which are found in many cell types including smooth muscles, neurons and endocrine cells. (wustl.edu)
  • While all affect the L type voltage gated calcium channel, the structure and site of interaction within the channel varies among the agents. (nih.gov)
  • There are four types of β subunits (β1- β4) that can associate with the pore forming Slo1 subunit to uniquely modulate the Ca2+ and voltage sensitive properties in BK channels. (wustl.edu)
  • In the first study, using a mutation that alters Ca2+ dependent activation, I show that in the presence of the β subunits, with the exception of β3b subunit, the mutation generally increased Ca2+ sensitivity to the same extent as in Slo1-only channels. (wustl.edu)
  • Violin plots show distribution of expression levels for Calcium activated potassium channel subunit (SMED30030583) in cells (dots) of each of the 12 neoblast clusters. (stowers.org)
  • Expression of Calcium activated potassium channel subunit (SMED30030583) in the t-SNE clustered sub-lethally irradiated X1 and X2 cells. (stowers.org)
  • We found that the A-type potassium channel subunit Kv4.2 is highly expressed in the dendritic regions of CA1 neurons in the hippocampus and, as one of the primary regulators of dendritic excitability, plays a pivotal role in information processing. (nih.gov)
  • Our lab used a combination of molecular, electrophysiological, and imaging techniques to show that Kv4.2, an A-type voltage-gated potassium channel subunit, controls action potential (AP) half-width, frequency-dependent AP broadening, and dendritic AP propagation. (nih.gov)
  • There are previous reports suggesting a role for calcium ions in the secretory response of adrenocortical cells to ACTH. (nih.gov)
  • Specifically we have used computational modeling, electrophysiology, and two-photon calcium imaging in mouse midbrain slices to show that this hyperpolarization-induced afterdepolarization (HI-ADP) depends on T-type, but not L-type calcium channels. (nih.gov)
  • Low-voltage-activated t-type calcium channels : proceedings from the International Electrophysiology meeting, Montpellier, 21-22 October 1996 / guest editors: Richard W. Tsien, Jean-Paul Clozel, Joël Nargeot. (who.int)
  • Most work on this calcium toxicity hypothesis implicates the L-type calcium channel. (nih.gov)
  • Because these channels can cause large calcium transients they may contribute to the vulnerability of specific SNc dopamine neurons in Parkinson's Disease. (nih.gov)
  • In general, these agents block the slow channel in the cell membrane and prevent calcium entry into the cell. (nursinganswers.net)
  • Current flowing through single Ca- and voltage-activated K channels has been recorded from cell-attached and inside-out excised membrane patches of cultured Y-1 adrenocortical cells. (nih.gov)
  • In intact cells, single-channel current amplitude and the time a channel stays in the open state increase with membrane depolarization. (nih.gov)
  • Therefore, it is possible that, as in other endocrine cells, these K channels modulate Ca influx across the plasma membrane and thus contribute to regulate steroid biosynthesis and release. (nih.gov)
  • Ion channels are the elementary excitable elements in the cell membranes of nerve, muscle, and many other cells where they produce and transduce electrical signals. (nih.gov)
  • This interaction that relies on specific Ca(v)3.2 molecular determinants, not only modulates T-type channel activity, but was also found essential to support low-threshold exocytosis upon Ca(v)3.2 channel expression in MPC 9/3L-AH chromaffin cells. (inserm.fr)
  • Signal of nerve impulses are transmitted to excitatory cells to induce action of organs via activation of Ca 2+ entry through voltage-gated Ca 2+ channels, which are classified based on their activation threshold into high- and low-voltage activated channels, expressed specifically for each organ. (mdpi.com)
  • Several reports have uncovered an unrecognized feature of T-type channels in the control of vesicular neurotransmitter and hormone release, a process so far thought to be mediated exclusively by high-voltage-activated calcium channels. (inserm.fr)
  • These channels are uniformly distributed in the plasma membrane, since one to four channels were seen in more than 99% of the patches isolated in this study. (nih.gov)
  • In spite of intense research, the signal that relays the store Ca(2+) content to CRAC channels in the plasma membrane, as well as the molecular identity of the Ca(2+) sensor within the stores, remains elusive. (ox.ac.uk)
  • Resolution of these issues would be greatly helped by the identification of the CRAC channel gene. (ox.ac.uk)
  • Store-operated Ca2+ entry (SOCE) through the Ca2+ release activated Ca2+ (CRAC) channels and mitochondrial Ca2+ uptake via the mitochondrial Ca2+ uniporter (MCU) complex are collective signaling mechanisms responsible for a variety of cellular functions. (cmos.org.tr)
  • In excised patches bathed in symmetrical 130 mM K solutions, single-channel conductance is 170 pS. (nih.gov)
  • More recently, we examined the role of A-type K+ channels in regulating synaptic plasticity, neuronal development and disease (1). (nih.gov)
  • If calcium influx is decreased, then norepinephrine vasoconstriction is reduced. (nursinganswers.net)
  • How do T-type calcium channels control low-threshold exocytosis? (inserm.fr)
  • However, the underlying molecular mechanisms linking T-type calcium channels to vesicular exocytosis have remained enigmatic. (inserm.fr)
  • Low-voltage-activated T-type calcium channels act as a major pathway for calcium entry near the resting membrane potential in a wide range of neuronal cell types. (inserm.fr)
  • In a recent study, we have reported that Ca(v)3.2 T-type channel forms a signaling complex with the neuronal Q-SNARE syntaxin-1A and SNAP-25. (inserm.fr)
  • However, the dendrites contain an abundance of ion channels that are involved in receiving, transforming, and relaying information in the dendrites, adding an additional layer of complexity to neuronal information processing. (nih.gov)
  • Although recent molecular cloning studies found that several families of voltage-gated K+ channel genes are expressed in the mammalian brain, information about the relationship between the protein products of these genes and their various neuronal functions is still lacking. (nih.gov)
  • In addition, we are investigating the role of dendritic voltage-gated channels in CNS disorders, including autism-spectrum disorder and Alzheimer's disease. (nih.gov)
  • With larger Ca concentrations, channel open probability increases and its voltage dependence is greater. (nih.gov)
  • This protein allows calcium to move into a nerve cell, and activates, deactivates, or stabilizes the electrical activity of the nerve. (sleep-disorders.net)
  • Aldrich lab's work is directed towards understanding the molecular and biophysical mechanisms of the function of ion channels. (nih.gov)
  • Aldrich lab is interested in the mechanisms by which these agents control the conformational changes that open and close the ion channel molecule. (nih.gov)
  • Collectively, these results provide a basis for future studies identifying the molecular basis for modulation by the β3 and β4 subunits in BK channels. (wustl.edu)
  • Functional variation of BK channels in different tissues is largely accounted by the association with accessory  subunits, which have tissue-specific distributions. (wustl.edu)
  • Alpha-2-delta calcium channel ligands are a class of drugs used for chronic, persistent restless legs syndrome (RLS) when iron supplements do not work. (sleep-disorders.net)
  • Do not take alpha-2-delta calcium channel ligands with other drugs that depress the central nervous system. (sleep-disorders.net)
  • In the second study, taking advantage of differential effect of 2 modulation on two BK channel orthologs, different chimeras were designed and coexpressed with β2 subunits. (wustl.edu)
  • This may occur because alpha sympathetic vasoconstriction is produced by enhanced calcium influx into the cell. (nursinganswers.net)
  • The present study was undertaken to explore the relative contributions of Cav3.2 T-type channels to mediating the antihyperalgesic activity of joint manipulation (JM) therapy . (bvsalud.org)