Acetylcholine: A neurotransmitter found at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, a subset of sympathetic effector junctions, and at many sites in the central nervous system.Receptors, Nicotinic: 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.Receptors, Cholinergic: Cell surface proteins that bind acetylcholine with high affinity and trigger intracellular changes influencing the behavior of cells. Cholinergic receptors are divided into two major classes, muscarinic and nicotinic, based originally on their affinity for nicotine and muscarine. Each group is further subdivided based on pharmacology, location, mode of action, and/or molecular biology.alpha7 Nicotinic Acetylcholine Receptor: A member of the NICOTINIC ACETYLCHOLINE RECEPTOR subfamily of the LIGAND-GATED ION CHANNEL family. It consists entirely of pentameric a7 subunits expressed in the CNS, autonomic nervous system, vascular system, lymphocytes and spleen.Bungarotoxins: Neurotoxic proteins from the venom of the banded or Formosan krait (Bungarus multicinctus, an elapid snake). alpha-Bungarotoxin blocks nicotinic acetylcholine receptors and has been used to isolate and study them; beta- and gamma-bungarotoxins act presynaptically causing acetylcholine release and depletion. Both alpha and beta forms have been characterized, the alpha being similar to the large, long or Type II neurotoxins from other elapid venoms.Torpedo: A genus of the Torpedinidae family consisting of several species. Members of this family have powerful electric organs and are commonly called electric rays.Vesicular Acetylcholine Transport Proteins: Vesicular amine transporter proteins that transport the neurotransmitter ACETYLCHOLINE into small SECRETORY VESICLES. Proteins of this family contain 12 transmembrane domains and exchange vesicular PROTONS for cytoplasmic acetylcholine.Receptors, Muscarinic: One of the two major classes of cholinergic receptors. Muscarinic receptors were originally defined by their preference for MUSCARINE over NICOTINE. There are several subtypes (usually M1, M2, M3....) that are characterized by their cellular actions, pharmacology, and molecular biology.Nicotinic Antagonists: Drugs that bind to nicotinic cholinergic receptors (RECEPTORS, NICOTINIC) and block the actions of acetylcholine or cholinergic agonists. Nicotinic antagonists block synaptic transmission at autonomic ganglia, the skeletal neuromuscular junction, and at central nervous system nicotinic synapses.Nicotinic Agonists: Drugs that bind to and activate nicotinic cholinergic receptors (RECEPTORS, NICOTINIC). Nicotinic agonists act at postganglionic nicotinic receptors, at neuroeffector junctions in the peripheral nervous system, and at nicotinic receptors in the central nervous system. Agents that function as neuromuscular depolarizing blocking agents are included here because they activate nicotinic receptors, although they are used clinically to block nicotinic transmission.Electric Organ: In about 250 species of electric fishes, modified muscle fibers forming disklike multinucleate plates arranged in stacks like batteries in series and embedded in a gelatinous matrix. A large torpedo ray may have half a million plates. Muscles in different parts of the body may be modified, i.e., the trunk and tail in the electric eel, the hyobranchial apparatus in the electric ray, and extrinsic eye muscles in the stargazers. Powerful electric organs emit pulses in brief bursts several times a second. They serve to stun prey and ward off predators. A large torpedo ray can produce of shock of more than 200 volts, capable of stunning a human. (Storer et al., General Zoology, 6th ed, p672)Atropine: An alkaloid, originally from Atropa belladonna, but found in other plants, mainly SOLANACEAE. Hyoscyamine is the 3(S)-endo isomer of atropine.Nicotine: Nicotine is highly toxic alkaloid. It is the prototypical agonist at nicotinic cholinergic receptors where it dramatically stimulates neurons and ultimately blocks synaptic transmission. Nicotine is also important medically because of its presence in tobacco smoke.Physostigmine: A cholinesterase inhibitor that is rapidly absorbed through membranes. It can be applied topically to the conjunctiva. It also can cross the blood-brain barrier and is used when central nervous system effects are desired, as in the treatment of severe anticholinergic toxicity.Neuromuscular Junction: The synapse between a neuron and a muscle.Carbachol: A slowly hydrolyzed CHOLINERGIC AGONIST that acts at both MUSCARINIC RECEPTORS and NICOTINIC RECEPTORS.Tubocurarine: A neuromuscular blocker and active ingredient in CURARE; plant based alkaloid of Menispermaceae.Cholinergic Agents: Any drug used for its actions on cholinergic systems. Included here are agonists and antagonists, drugs that affect the life cycle of ACETYLCHOLINE, and drugs that affect the survival of cholinergic neurons. The term cholinergic agents is sometimes still used in the narrower sense of MUSCARINIC AGONISTS, although most modern texts discourage that usage.Muscarinic Antagonists: Drugs that bind to but do not activate MUSCARINIC RECEPTORS, thereby blocking the actions of endogenous ACETYLCHOLINE or exogenous agonists. Muscarinic antagonists have widespread effects including actions on the iris and ciliary muscle of the eye, the heart and blood vessels, secretions of the respiratory tract, GI system, and salivary glands, GI motility, urinary bladder tone, and the central nervous system.Choline: A basic constituent of lecithin that is found in many plants and animal organs. It is important as a precursor of acetylcholine, as a methyl donor in various metabolic processes, and in lipid metabolism.Cholinesterase Inhibitors: Drugs that inhibit cholinesterases. The neurotransmitter ACETYLCHOLINE is rapidly hydrolyzed, and thereby inactivated, by cholinesterases. When cholinesterases are inhibited, the action of endogenously released acetylcholine at cholinergic synapses is potentiated. Cholinesterase inhibitors are widely used clinically for their potentiation of cholinergic inputs to the gastrointestinal tract and urinary bladder, the eye, and skeletal muscles; they are also used for their effects on the heart and the central nervous system.Acetylcholinesterase: An enzyme that catalyzes the hydrolysis of ACETYLCHOLINE to CHOLINE and acetate. In the CNS, this enzyme plays a role in the function of peripheral neuromuscular junctions. EC 3.1.1.7.Receptor, Muscarinic M2: A specific subtype of muscarinic receptor found in the lower BRAIN, the HEART and in SMOOTH MUSCLE-containing organs. Although present in smooth muscle the M2 muscarinic receptor appears not to be involved in contractile responses.Vasodilation: The physiological widening of BLOOD VESSELS by relaxing the underlying VASCULAR SMOOTH MUSCLE.Muscarinic Agonists: Drugs that bind to and activate muscarinic cholinergic receptors (RECEPTORS, MUSCARINIC). Muscarinic agonists are most commonly used when it is desirable to increase smooth muscle tone, especially in the GI tract, urinary bladder and the eye. They may also be used to reduce heart rate.Receptor, Muscarinic M1: A specific subtype of muscarinic receptor that has a high affinity for the drug PIRENZEPINE. It is found in the peripheral GANGLIA where it signals a variety of physiological functions such as GASTRIC ACID secretion and BRONCHOCONSTRICTION. This subtype of muscarinic receptor is also found in neuronal tissues including the CEREBRAL CORTEX and HIPPOCAMPUS where it mediates the process of MEMORY and LEARNING.Myasthenia Gravis: A disorder of neuromuscular transmission characterized by weakness of cranial and skeletal muscles. Autoantibodies directed against acetylcholine receptors damage the motor endplate portion of the NEUROMUSCULAR JUNCTION, impairing the transmission of impulses to skeletal muscles. Clinical manifestations may include diplopia, ptosis, and weakness of facial, bulbar, respiratory, and proximal limb muscles. The disease may remain limited to the ocular muscles. THYMOMA is commonly associated with this condition. (Adams et al., Principles of Neurology, 6th ed, p1459)Vasodilator Agents: Drugs used to cause dilation of the blood vessels.Receptor, Muscarinic M3: A subclass of muscarinic receptor that mediates cholinergic-induced contraction in a variety of SMOOTH MUSCLES.Parasympathomimetics: Drugs that mimic the effects of parasympathetic nervous system activity. Included here are drugs that directly stimulate muscarinic receptors and drugs that potentiate cholinergic activity, usually by slowing the breakdown of acetylcholine (CHOLINESTERASE INHIBITORS). Drugs that stimulate both sympathetic and parasympathetic postganglionic neurons (GANGLIONIC STIMULANTS) are not included here.Motor Endplate: The specialized postsynaptic region of a muscle cell. The motor endplate is immediately across the synaptic cleft from the presynaptic axon terminal. Among its anatomical specializations are junctional folds which harbor a high density of cholinergic receptors.Muscles: Contractile tissue that produces movement in animals.Mecamylamine: A nicotinic antagonist that is well absorbed from the gastrointestinal tract and crosses the blood-brain barrier. Mecamylamine has been used as a ganglionic blocker in treating hypertension, but, like most ganglionic blockers, is more often used now as a research tool.Choline O-Acetyltransferase: An enzyme that catalyzes the formation of acetylcholine from acetyl-CoA and choline. EC 2.3.1.6.Aconitine: A C19 norditerpenoid alkaloid (DITERPENES) from the root of ACONITUM plants. It activates VOLTAGE-GATED SODIUM CHANNELS. It has been used to induce ARRHYTHMIAS in experimental animals and it has antiinflammatory and antineuralgic properties.Nitroprusside: A powerful vasodilator used in emergencies to lower blood pressure or to improve cardiac function. It is also an indicator for free sulfhydryl groups in proteins.Dose-Response Relationship, Drug: The relationship between the dose of an administered drug and the response of the organism to the drug.Conotoxins: Peptide neurotoxins from the marine fish-hunting snails of the genus CONUS. They contain 13 to 29 amino acids which are strongly basic and are highly cross-linked by disulfide bonds. There are three types of conotoxins, omega-, alpha-, and mu-. OMEGA-CONOTOXINS inhibit voltage-activated entry of calcium into the presynaptic membrane and therefore the release of ACETYLCHOLINE. Alpha-conotoxins inhibit the postsynaptic acetylcholine receptor. Mu-conotoxins prevent the generation of muscle action potentials. (From Concise Encyclopedia Biochemistry and Molecular Biology, 3rd ed)Cholinergic Agonists: Drugs that bind to and activate cholinergic receptors.AzocinesParasympatholytics: Agents that inhibit the actions of the parasympathetic nervous system. The major group of drugs used therapeutically for this purpose is the MUSCARINIC ANTAGONISTS.Oxotremorine: A non-hydrolyzed muscarinic agonist used as a research tool.Cobra Neurotoxin Proteins: Toxins, contained in cobra (Naja) venom that block cholinergic receptors; two specific proteins have been described, the small (short, Type I) and the large (long, Type II) which also exist in other Elapid venoms.Guinea Pigs: 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.Parasympathetic Nervous System: The craniosacral division of the autonomic nervous system. The cell bodies of the parasympathetic preganglionic fibers are in brain stem nuclei and in the sacral spinal cord. They synapse in cranial autonomic ganglia or in terminal ganglia near target organs. The parasympathetic nervous system generally acts to conserve resources and restore homeostasis, often with effects reciprocal to the sympathetic nervous system.Endothelium, Vascular: Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.Quinuclidinyl Benzilate: A high-affinity muscarinic antagonist commonly used as a tool in animal and tissue studies.Agrin: A protein component of the synaptic basal lamina. It has been shown to induce clustering of acetylcholine receptors on the surface of muscle fibers and other synaptic molecules in both synapse regeneration and development.Membrane Potentials: 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).Cholinergic Fibers: Nerve fibers liberating acetylcholine at the synapse after an impulse.Hexamethonium Compounds: Compounds containing the hexamethylenebis(trimethylammonium) cation. Members of this group frequently act as antihypertensive agents and selective ganglionic blocking agents.Muscle Contraction: 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.N-Methylscopolamine: A muscarinic antagonist used to study binding characteristics of muscarinic cholinergic receptors.Electric Stimulation: Use of electric potential or currents to elicit biological responses.Hemicholinium 3: A potent inhibitor of the high affinity uptake system for CHOLINE. It has less effect on the low affinity uptake system. Since choline is one of the components of ACETYLCHOLINE, treatment with hemicholinium can deplete acetylcholine from cholinergic terminals. Hemicholinium 3 is commonly used as a research tool in animal and in vitro experiments.Dihydro-beta-Erythroidine: Dihydro analog of beta-erythroidine, which is isolated from the seeds and other plant parts of Erythrina sp. Leguminosae. It is an alkaloid with curarimimetic properties.Cholinergic Antagonists: Drugs that bind to but do not activate CHOLINERGIC RECEPTORS, thereby blocking the actions of ACETYLCHOLINE or cholinergic agonists.Muscle Denervation: The resection or removal of the innervation of a muscle or muscle tissue.Bicyclo Compounds, Heterocyclic: A class of saturated compounds consisting of two rings only, having two or more atoms in common, containing at least one hetero atom, and that take the name of an open chain hydrocarbon containing the same total number of atoms. (From Riguady et al., Nomenclature of Organic Chemistry, 1979, p31)Scopolamine Hydrobromide: An alkaloid from SOLANACEAE, especially DATURA and SCOPOLIA. Scopolamine and its quaternary derivatives act as antimuscarinics like ATROPINE, but may have more central nervous system effects. Among the many uses are as an anesthetic premedication, in URINARY INCONTINENCE, in MOTION SICKNESS, as an antispasmodic, and as a mydriatic and cycloplegic.Neostigmine: A cholinesterase inhibitor used in the treatment of myasthenia gravis and to reverse the effects of muscle relaxants such as gallamine and tubocurarine. Neostigmine, unlike PHYSOSTIGMINE, does not cross the blood-brain barrier.Electrophorus: A genus of fish, in the family GYMNOTIFORMES, capable of producing an electric shock that immobilizes fish and other prey. The species Electrophorus electricus is also known as the electric eel, though it is not a true eel.Synaptic Transmission: 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.Muscle, Smooth: 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)QuinolizinesGallamine Triethiodide: A synthetic nondepolarizing blocking drug. The actions of gallamine triethiodide are similar to those of TUBOCURARINE, but this agent blocks the cardiac vagus and may cause sinus tachycardia and, occasionally, hypertension and increased cardiac output. It should be used cautiously in patients at risk from increased heart rate but may be preferred for patients with bradycardia. (From AMA Drug Evaluations Annual, 1992, p198)Receptor, Muscarinic M4: A specific subtype of muscarinic receptor found in the CORPUS STRIATUM and the LUNG. It has similar receptor binding specificities to MUSCARINIC RECEPTOR M1 and MUSCARINIC RECEPTOR M2.Iontophoresis: Therapeutic introduction of ions of soluble salts into tissues by means of electric current. In medical literature it is commonly used to indicate the process of increasing the penetration of drugs into surface tissues by the application of electric current. It has nothing to do with ION EXCHANGE; AIR IONIZATION nor PHONOPHORESIS, none of which requires current.Nitric Oxide: A free radical gas produced endogenously by a variety of mammalian cells, synthesized from ARGININE by NITRIC OXIDE SYNTHASE. Nitric oxide is one of the ENDOTHELIUM-DEPENDENT RELAXING FACTORS released by the vascular endothelium and mediates VASODILATION. It also inhibits platelet aggregation, induces disaggregation of aggregated platelets, and inhibits platelet adhesion to the vascular endothelium. Nitric oxide activates cytosolic GUANYLATE CYCLASE and thus elevates intracellular levels of CYCLIC GMP.Neurons: 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.Decamethonium Compounds: Compounds that contain the decamethylenebis(trimethyl)ammonium radical. These compounds frequently act as neuromuscular depolarizing agents.Pirenzepine: An antimuscarinic agent that inhibits gastric secretion at lower doses than are required to affect gastrointestinal motility, salivary, central nervous system, cardiovascular, ocular, and urinary function. It promotes the healing of duodenal ulcers and due to its cytoprotective action is beneficial in the prevention of duodenal ulcer recurrence. It also potentiates the effect of other antiulcer agents such as CIMETIDINE and RANITIDINE. It is generally well tolerated by patients.Calcium: 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.Norepinephrine: Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in the brain arising from the locus ceruleus. It is also found in plants and is used pharmacologically as a sympathomimetic.Amphibian Venoms: Venoms produced by frogs, toads, salamanders, etc. The venom glands are usually on the skin of the back and contain cardiotoxic glycosides, cholinolytics, and a number of other bioactive materials, many of which have been characterized. The venoms have been used as arrow poisons and include bufogenin, bufotoxin, bufagin, bufotalin, histrionicotoxins, and pumiliotoxin.Dimethylphenylpiperazinium Iodide: A selective nicotinic cholinergic agonist used as a research tool. DMPP activates nicotinic receptors in autonomic ganglia but has little effect at the neuromuscular junction.Synaptic Membranes: Cell membranes associated with synapses. Both presynaptic and postsynaptic membranes are included along with their integral or tightly associated specializations for the release or reception of transmitters.Xenopus laevis: 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.Ion Channels: 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.Ileum: The distal and narrowest portion of the SMALL INTESTINE, between the JEJUNUM and the ILEOCECAL VALVE of the LARGE INTESTINE.Electrophysiology: 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.Rats, Sprague-Dawley: 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.Curare: Plant extracts from several species, including genera STRYCHNOS and Chondodendron, which contain TETRAHYDROISOQUINOLINES that produce PARALYSIS of skeletal muscle. These extracts are toxic and must be used with the administration of artificial respiration.Muscarine: A toxic alkaloid found in Amanita muscaria (fly fungus) and other fungi of the Inocybe species. It is the first parasympathomimetic substance ever studied and causes profound parasympathetic activation that may end in convulsions and death. The specific antidote is atropine.Muscle Relaxation: That phase of a muscle twitch during which a muscle returns to a resting position.Hexamethonium: A nicotinic cholinergic antagonist often referred to as the prototypical ganglionic blocker. It is poorly absorbed from the gastrointestinal tract and does not cross the blood-brain barrier. It has been used for a variety of therapeutic purposes including hypertension but, like the other ganglionic blockers, it has been replaced by more specific drugs for most purposes, although it is widely used a research tool.Neurotransmitter Agents: 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.Myasthenic Syndromes, Congenital: A heterogeneous group of disorders characterized by a congenital defect in neuromuscular transmission at the NEUROMUSCULAR JUNCTION. This includes presynaptic, synaptic, and postsynaptic disorders (that are not of autoimmune origin). The majority of these diseases are caused by mutations of various subunits of the nicotinic acetylcholine receptor (RECEPTORS, NICOTINIC) on the postsynaptic surface of the junction. (From Arch Neurol 1999 Feb;56(2):163-7)Receptor, Muscarinic M5: A specific subtype of muscarinic receptor found in a variety of locations including the SALIVARY GLANDS and the SUBSTANTIA NIGRA and VENTRAL TEGMENTAL AREA of the BRAIN.Kinetics: The rate dynamics in chemical or physical systems.Ganglia, Autonomic: Clusters of neurons and their processes in the autonomic nervous system. In the autonomic ganglia, the preganglionic fibers from the central nervous system synapse onto the neurons whose axons are the postganglionic fibers innervating target organs. The ganglia also contain intrinsic neurons and supporting cells and preganglionic fibers passing through to other ganglia.Microdialysis: A technique for measuring extracellular concentrations of substances in tissues, usually in vivo, by means of a small probe equipped with a semipermeable membrane. Substances may also be introduced into the extracellular space through the membrane.Ganglia, Parasympathetic: Ganglia of the parasympathetic nervous system, including the ciliary, pterygopalatine, submandibular, and otic ganglia in the cranial region and intrinsic (terminal) ganglia associated with target organs in the thorax and abdomen.Potassium: 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.Patch-Clamp Techniques: 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.CholinesterasesNerve Endings: Branch-like terminations of NERVE FIBERS, sensory or motor NEURONS. Endings of sensory neurons are the beginnings of afferent pathway to the CENTRAL NERVOUS SYSTEM. Endings of motor neurons are the terminals of axons at the muscle cells. Nerve endings which release neurotransmitters are called PRESYNAPTIC TERMINALS.Piperidines: A family of hexahydropyridines.Biological Factors: Endogenously-synthesized compounds that influence biological processes not otherwise classified under ENZYMES; HORMONES or HORMONE ANTAGONISTS.Oocytes: 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).Forearm: Part of the arm in humans and primates extending from the ELBOW to the WRIST.Pyridines: Compounds with a six membered aromatic ring containing NITROGEN. The saturated version is PIPERIDINES.Receptor Aggregation: Chemically stimulated aggregation of cell surface receptors, which potentiates the action of the effector cell.Protein Subunits: 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.Tetrodotoxin: 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.Synapses: 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.Diaphragm: The musculofibrous partition that separates the THORACIC CAVITY from the ABDOMINAL CAVITY. Contraction of the diaphragm increases the volume of the thoracic cavity aiding INHALATION.omega-N-Methylarginine: A competitive inhibitor of nitric oxide synthetase.Rats, Wistar: A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.Time Factors: Elements of limited time intervals, contributing to particular results or situations.Cells, Cultured: 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.Action Potentials: Abrupt changes in the membrane potential that sweep along the CELL MEMBRANE of excitable cells in response to excitation stimuli.Vasoconstriction: The physiological narrowing of BLOOD VESSELS by contraction of the VASCULAR SMOOTH MUSCLE.Cholinergic Neurons: Neurons whose primary neurotransmitter is ACETYLCHOLINE.Nitroarginine: An inhibitor of nitric oxide synthetase which has been shown to prevent glutamate toxicity. Nitroarginine has been experimentally tested for its ability to prevent ammonia toxicity and ammonia-induced alterations in brain energy and ammonia metabolites. (Neurochem Res 1995:200(4):451-6)Methacholine Compounds: A group of compounds that are derivatives of beta-methylacetylcholine (methacholine).Rabbits: 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.Vasoconstrictor Agents: Drugs used to cause constriction of the blood vessels.Amino Acid Sequence: 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.Ganglionic Stimulants: Agents that mimic neural transmission by stimulation of the nicotinic receptors on postganglionic autonomic neurons. Drugs that indirectly augment ganglionic transmission by increasing the release or slowing the breakdown of acetylcholine or by non-nicotinic effects on postganglionic neurons are not included here nor are the nonspecific cholinergic agonists.Serotonin: A biochemical messenger and regulator, synthesized from the essential amino acid L-TRYPTOPHAN. In humans it is found primarily in the central nervous system, gastrointestinal tract, and blood platelets. Serotonin mediates several important physiological functions including neurotransmission, gastrointestinal motility, hemostasis, and cardiovascular integrity. Multiple receptor families (RECEPTORS, SEROTONIN) explain the broad physiological actions and distribution of this biochemical mediator.Histamine: An amine derived by enzymatic decarboxylation of HISTIDINE. It is a powerful stimulant of gastric secretion, a constrictor of bronchial smooth muscle, a vasodilator, and also a centrally acting neurotransmitter.Synaptosomes: Pinched-off nerve endings and their contents of vesicles and cytoplasm together with the attached subsynaptic area of the membrane of the post-synaptic cell. They are largely artificial structures produced by fractionation after selective centrifugation of nervous tissue homogenates.Neuromuscular Depolarizing Agents: Drugs that interrupt transmission at the skeletal neuromuscular junction by causing sustained depolarization of the motor end plate. These agents are primarily used as adjuvants in surgical anesthesia to cause skeletal muscle relaxation.Binding Sites: The parts of a macromolecule that directly participate in its specific combination with another molecule.Bradykinin: A nonapeptide messenger that is enzymatically produced from KALLIDIN in the blood where it is a potent but short-lived agent of arteriolar dilation and increased capillary permeability. Bradykinin is also released from MAST CELLS during asthma attacks, from gut walls as a gastrointestinal vasodilator, from damaged tissues as a pain signal, and may be a neurotransmitter.Binding, Competitive: The interaction of two or more substrates or ligands with the same binding site. The displacement of one by the other is used in quantitative and selective affinity measurements.Molecular Sequence Data: 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.Cats: The domestic cat, Felis catus, of the carnivore family FELIDAE, comprising over 30 different breeds. The domestic cat is descended primarily from the wild cat of Africa and extreme southwestern Asia. Though probably present in towns in Palestine as long ago as 7000 years, actual domestication occurred in Egypt about 4000 years ago. (From Walker's Mammals of the World, 6th ed, p801)Quaternary Ammonium Compounds: Derivatives of ammonium compounds, NH4+ Y-, in which all four of the hydrogens bonded to nitrogen have been replaced with hydrocarbyl groups. These are distinguished from IMINES which are RN=CR2.Xenopus: An aquatic genus of the family, Pipidae, occurring in Africa and distinguished by having black horny claws on three inner hind toes.Galantamine: A benzazepine derived from norbelladine. It is found in GALANTHUS and other AMARYLLIDACEAE. It is a cholinesterase inhibitor that has been used to reverse the muscular effects of GALLAMINE TRIETHIODIDE and TUBOCURARINE and has been studied as a treatment for ALZHEIMER DISEASE and other central nervous system disorders.Snakes: Limbless REPTILES of the suborder Serpentes.Trachea: The cartilaginous and membranous tube descending from the larynx and branching into the right and left main bronchi.Anabasine: A piperidine botanical insecticide.Brain: 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.Nitroglycerin: A volatile vasodilator which relieves ANGINA PECTORIS by stimulating GUANYLATE CYCLASE and lowering cytosolic calcium. It is also sometimes used for TOCOLYSIS and explosives.Mesenteric Arteries: Arteries which arise from the abdominal aorta and distribute to most of the intestines.Proadifen: An inhibitor of drug metabolism and CYTOCHROME P-450 ENZYME SYSTEM activity.Vasomotor System: The neural systems which act on VASCULAR SMOOTH MUSCLE to control blood vessel diameter. The major neural control is through the sympathetic nervous system.Vagus Nerve: The 10th cranial nerve. The vagus is a mixed nerve which contains somatic afferents (from skin in back of the ear and the external auditory meatus), visceral afferents (from the pharynx, larynx, thorax, and abdomen), parasympathetic efferents (to the thorax and abdomen), and efferents to striated muscle (of the larynx and pharynx).Ganglionic Blockers: Agents having as their major action the interruption of neural transmission at nicotinic receptors on postganglionic autonomic neurons. Because their actions are so broad, including blocking of sympathetic and parasympathetic systems, their therapeutic use has been largely supplanted by more specific drugs. They may still be used in the control of blood pressure in patients with acute dissecting aortic aneurysm and for the induction of hypotension in surgery.Potassium Chloride: 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.Dogs: 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)Myenteric Plexus: One of two ganglionated neural networks which together form the ENTERIC NERVOUS SYSTEM. The myenteric (Auerbach's) plexus is located between the longitudinal and circular muscle layers of the gut. Its neurons project to the circular muscle, to other myenteric ganglia, to submucosal ganglia, or directly to the epithelium, and play an important role in regulating and patterning gut motility. (From FASEB J 1989;3:127-38)Cell Membrane: The lipid- and protein-containing, selectively permeable membrane that surrounds the cytoplasm in prokaryotic and eukaryotic cells.Alkaloids: Organic nitrogenous bases. Many alkaloids of medical importance occur in the animal and vegetable kingdoms, and some have been synthesized. (Grant & Hackh's Chemical Dictionary, 5th ed)Nitric Oxide Synthase: An NADPH-dependent enzyme that catalyzes the conversion of L-ARGININE and OXYGEN to produce CITRULLINE and NITRIC OXIDE.Paraoxon: An organophosphate cholinesterase inhibitor that is used as a pesticide.AzetidinesAorta, Thoracic: The portion of the descending aorta proceeding from the arch of the aorta and extending to the DIAPHRAGM, eventually connecting to the ABDOMINAL AORTA.Radioligand Assay: Quantitative determination of receptor (binding) proteins in body fluids or tissue using radioactively labeled binding reagents (e.g., antibodies, intracellular receptors, plasma binders).NG-Nitroarginine Methyl Ester: A non-selective inhibitor of nitric oxide synthase. It has been used experimentally to induce hypertension.Rana pipiens: A highly variable species of the family Ranidae in Canada, the United States and Central America. It is the most widely used Anuran in biomedical research.Arginine: An essential amino acid that is physiologically active in the L-form.Indomethacin: A non-steroidal anti-inflammatory agent (NSAID) that inhibits the enzyme cyclooxygenase necessary for the formation of prostaglandins and other autacoids. It also inhibits the motility of polymorphonuclear leukocytes.TritiumDrug Interactions: The action of a drug that may affect the activity, metabolism, or toxicity of another drug.QuinuclidinesCell Line: Established cell cultures that have the potential to propagate indefinitely.Phenylephrine: An alpha-1 adrenergic agonist used as a mydriatic, nasal decongestant, and cardiotonic agent.Coronary Vessels: The veins and arteries of the HEART.Ion Channel Gating: 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.Neuromuscular Blocking Agents: Drugs that interrupt transmission of nerve impulses at the skeletal neuromuscular junction. They can be of two types, competitive, stabilizing blockers (NEUROMUSCULAR NONDEPOLARIZING AGENTS) or noncompetitive, depolarizing agents (NEUROMUSCULAR DEPOLARIZING AGENTS). Both prevent acetylcholine from triggering the muscle contraction and they are used as anesthesia adjuvants, as relaxants during electroshock, in convulsive states, etc.Neurotoxins: Toxic substances from microorganisms, plants or animals that interfere with the functions of the nervous system. Most venoms contain neurotoxic substances. Myotoxins are included in this concept.Electric Conductivity: The ability of a substrate to allow the passage of ELECTRONS.Macromolecular Substances: Compounds and molecular complexes that consist of very large numbers of atoms and are generally over 500 kDa in size. In biological systems macromolecular substances usually can be visualized using ELECTRON MICROSCOPY and are distinguished from ORGANELLES by the lack of a membrane structure.Ligands: A molecule that binds to another molecule, used especially to refer to a small molecule that binds specifically to a larger molecule, e.g., an antigen binding to an antibody, a hormone or neurotransmitter binding to a receptor, or a substrate or allosteric effector binding to an enzyme. Ligands are also molecules that donate or accept a pair of electrons to form a coordinate covalent bond with the central metal atom of a coordination complex. (From Dorland, 27th ed)Enzyme Inhibitors: Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.Regional Blood Flow: The flow of BLOOD through or around an organ or region of the body.Allosteric Regulation: The modification of the reactivity of ENZYMES by the binding of effectors to sites (ALLOSTERIC SITES) on the enzymes other than the substrate BINDING SITES.Hippocampus: 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.Muscle, Smooth, Vascular: The nonstriated involuntary muscle tissue of blood vessels.Substance P: An eleven-amino acid neurotransmitter that appears in both the central and peripheral nervous systems. It is involved in transmission of PAIN, causes rapid contractions of the gastrointestinal smooth muscle, and modulates inflammatory and immune responses.Chick Embryo: The developmental entity of a fertilized chicken egg (ZYGOTE). The developmental process begins about 24 h before the egg is laid at the BLASTODISC, a small whitish spot on the surface of the EGG YOLK. After 21 days of incubation, the embryo is fully developed before hatching.Arterioles: The smallest divisions of the arteries located between the muscular arteries and the capillaries.Sweat Glands: Sweat-producing structures that are embedded in the DERMIS. Each gland consists of a single tube, a coiled body, and a superficial duct.Dopamine: One of the catecholamine NEUROTRANSMITTERS in the brain. It is derived from TYROSINE and is the precursor to NOREPINEPHRINE and EPINEPHRINE. Dopamine is a major transmitter in the extrapyramidal system of the brain, and important in regulating movement. A family of receptors (RECEPTORS, DOPAMINE) mediate its action.Cerebral Cortex: The thin layer of GRAY MATTER on the surface of the CEREBRAL HEMISPHERES that develops from the TELENCEPHALON and folds into gyri and sulchi. It reaches its highest development in humans and is responsible for intellectual faculties and higher mental functions.Myasthenia Gravis, Autoimmune, Experimental: Any autoimmune animal disease model used in the study of MYASTHENIA GRAVIS. Injection with purified neuromuscular junction acetylcholine receptor (AChR) (see RECEPTORS, CHOLINERGIC) components results in a myasthenic syndrome that has acute and chronic phases. The motor endplate pathology, loss of acetylcholine receptors, presence of circulating anti-AChR antibodies, and electrophysiologic changes make this condition virtually identical to human myasthenia gravis. Passive transfer of AChR antibodies or lymphocytes from afflicted animals to normals induces passive transfer experimental autoimmune myasthenia gravis. (From Joynt, Clinical Neurology, 1997, Ch 54, p3)Coronary Vasospasm: Spasm of the large- or medium-sized coronary arteries.Ganglia, Sympathetic: Ganglia of the sympathetic nervous system including the paravertebral and the prevertebral ganglia. Among these are the sympathetic chain ganglia, the superior, middle, and inferior cervical ganglia, and the aorticorenal, celiac, and stellate ganglia.Benzylidene Compounds: Compounds containing the PhCH= radical.QuinoxalinesRats, Inbred Strains: Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations or by parent x offspring matings carried out with certain restrictions. This also includes animals with a long history of closed colony breeding.Anura: An order of the class Amphibia, which includes several families of frogs and toads. They are characterized by well developed hind limbs adapted for jumping, fused head and trunk and webbed toes. The term "toad" is ambiguous and is properly applied only to the family Bufonidae.Phencyclidine: A hallucinogen formerly used as a veterinary anesthetic, and briefly as a general anesthetic for humans. Phencyclidine is similar to KETAMINE in structure and in many of its effects. Like ketamine, it can produce a dissociative state. It exerts its pharmacological action through inhibition of NMDA receptors (RECEPTORS, N-METHYL-D-ASPARTATE). As a drug of abuse, it is known as PCP and Angel Dust.Isoproterenol: Isopropyl analog of EPINEPHRINE; beta-sympathomimetic that acts on the heart, bronchi, skeletal muscle, alimentary tract, etc. It is used mainly as bronchodilator and heart stimulant.Catecholamines: A general class of ortho-dihydroxyphenylalkylamines derived from tyrosine.gamma-Aminobutyric Acid: The most common inhibitory neurotransmitter in the central nervous system.Fishes: A group of cold-blooded, aquatic vertebrates having gills, fins, a cartilaginous or bony endoskeleton, and elongated bodies covered with scales.Motor Neurons: Neurons which activate MUSCLE CELLS.Arecoline: An alkaloid obtained from the betel nut (Areca catechu), fruit of a palm tree. It is an agonist at both muscarinic and nicotinic acetylcholine receptors. It is used in the form of various salts as a ganglionic stimulant, a parasympathomimetic, and a vermifuge, especially in veterinary practice. It has been used as a euphoriant in the Pacific Islands.Pilocarpine: A slowly hydrolyzed muscarinic agonist with no nicotinic effects. Pilocarpine is used as a miotic and in the treatment of glaucoma.Muscle, Skeletal: A subtype of striated muscle, attached by TENDONS to the SKELETON. Skeletal muscles are innervated and their movement can be consciously controlled. They are also called voluntary muscles.Protein Binding: 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.Nootropic Agents: Drugs used to specifically facilitate learning or memory, particularly to prevent the cognitive deficits associated with dementias. These drugs act by a variety of mechanisms. While no potent nootropic drugs have yet been accepted for general use, several are being actively investigated.Procaine: A local anesthetic of the ester type that has a slow onset and a short duration of action. It is mainly used for infiltration anesthesia, peripheral nerve block, and spinal block. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1016).Cobra Venoms: Venoms from snakes of the genus Naja (family Elapidae). They contain many specific proteins that have cytotoxic, hemolytic, neurotoxic, and other properties. Like other elapid venoms, they are rich in enzymes. They include cobramines and cobralysins.Stimulation, Chemical: The increase in a measurable parameter of a PHYSIOLOGICAL PROCESS, including cellular, microbial, and plant; immunological, cardiovascular, respiratory, reproductive, urinary, digestive, neural, musculoskeletal, ocular, and skin physiological processes; or METABOLIC PROCESS, including enzymatic and other pharmacological processes, by a drug or other chemical.Blood Pressure: PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.

Inhibitory innervation of cat sphincter of Oddi. (1/8871)

1 Electrical stimulation with trains of 0.1-0.2 ms pulses of the cat isolated sphincter of Oddi inhibited the spontaneous contractile activity and lowered base-line tension considerably. A contraction usually followed the period of stimulation. 2 These inhibitory effects were prevented by tetrodotoxin 0.1-0.5 mug/ml but were not reduced by hexamethonilm, morphine, or blockade of alpha- or beta-adrenoreceptors of cholinoceptors with phenoxy-benzamine propranolol or atropine, respectively. 3 Adenosine-5'-triphosphate (ATP) and adenosine-5'-diphosphate (ADP) inhibited the spontaneous sphincter activity and caused relaxation thus mimicking the effects of the C-terminal octapeptide of cholecystokinin (C8-CCK), isoprenaline and prostaglandin E1 and E2. 4 ATP alone (greater than 100 mug/ml) or ATP (greater than 10 mug/ml) plus dipyridamole (1 mug/ml), relaxed the sphincter to the same degrees as did the field stimulation. 5 In sphincter maximally contracted by acetylcholine, the effect of stimulation was more marked than that recorded in uncontracted preparations. 6 The present findings suggest that the sphincter of Oddi receives inhibitory nerves that are neither cholinergic nor adrenergic.  (+info)

A comparison of affinity constants for muscarine-sensitive acetylcholine receptors in guinea-pig atrial pacemaker cells at 29 degrees C and in ileum at 29 degrees C and 37 degrees C. (2/8871)

1 The affinity of 17 compounds for muscarine-sensitive acetylcholine receptors in atrial pacemaker cells and ileum of the guinea-pig has been measured at 29 degrees C in Ringer-Locke solution. Measurements were also made at 37 degrees C with 7 of them. 2 Some of the compounds had much higher affinity for the receptors in the ileum than for those in the atria. For the most selective compound, 4-diphenylacetoxy-N-methylpiperidine methiodide, the difference was approximately 20-fold. The receptors in the atria are therefore different the structure from those in the ileum. 3 The effect of temperature on affinity are not the same for all the compounds, tested indicating different enthalpies and entropies of adsorption and accounting for some of the difficulty experienced in predicting the affinity of new compounds.  (+info)

Modulation of long-term synaptic depression in visual cortex by acetylcholine and norepinephrine. (3/8871)

In a slice preparation of rat visual cortex, we discovered that paired-pulse stimulation (PPS) elicits a form of homosynaptic long-term depression (LTD) in the superficial layers when carbachol (CCh) or norepinephrine (NE) is applied concurrently. PPS by itself, or CCh and NE in the absence of synaptic stimulation, produced no lasting change. The LTD induced by PPS in the presence of NE or CCh is of comparable magnitude with that obtained with prolonged low-frequency stimulation (LFS) but requires far fewer stimulation pulses (40 vs 900). The cholinergic facilitation of LTD was blocked by atropine and pirenzepine, suggesting involvement of M1 receptors. The noradrenergic facilitation of LTD was blocked by urapidil and was mimicked by methoxamine, suggesting involvement of alpha1 receptors. beta receptor agonists and antagonists were without effect. Induction of LTD by PPS was inhibited by NMDA receptor blockers (completely in the case of NE; partially in the case of CCh), suggesting that one action of the modulators is to control the gain of NMDA receptor-dependent homosynaptic LTD in visual cortex. We propose that this is a mechanism by which cholinergic and noradrenergic inputs to the neocortex modulate naturally occurring receptive field plasticity.  (+info)

Endothelial function in Marfan syndrome: selective impairment of flow-mediated vasodilation. (4/8871)

BACKGROUND: The cardiovascular complications of Marfan syndrome arise due to alterations in the structural and functional properties of fibrillin, a constituent of vascular connective tissues. Fibrillin-containing microfibrils are closely associated with arterial endothelial cells, indicating a possible functional role for fibrillin in the endothelium. Plasma concentrations of endothelial cell products are elevated in Marfan subjects, which indirectly indicates endothelial dysfunction. This study directly assessed flow- and agonist-mediated endothelium-dependent brachial artery reactivity in Marfan subjects. METHODS AND RESULTS: In 20 Marfan and 20 control subjects, brachial artery diameter, blood flow, and blood pressure were measured by ultrasonic wall tracking, Doppler ultrasound, and photoplethysmography, respectively. Measurements were taken during hand hyperemia (a stimulus for endothelium-derived nitric oxide [NO] release in the upstream brachial artery) and after sublingual administration of the endothelium-independent vasodilator nitroglycerin. In 9 Marfan and 6 control subjects, the above parameters were also assessed during intra-arterial infusions of acetylcholine and bradykinin (agonists that stimulate NO production) and NG-monomethyl-L-arginine (L-NMMA, an inhibitor of NO production). Flow-mediated responses differed markedly between Marfan and control subjects (-1.6+/-3.5% versus 6. 50+/-4.1%, respectively; P<0.0001), whereas nitroglycerin produced similar vasodilation (14.2+/-5.7% versus 15.2+/-7.8%; P=NS). Agonist-induced vasodilation to incremental intra-arterial infusions of acetylcholine and bradykinin were not significantly different between Marfan and control subjects, and intra-arterial L-NMMA produced similar reductions in brachial artery diameter in both groups. CONCLUSIONS: These data demonstrate impaired flow-mediated but preserved agonist-mediated endothelium-dependent vasodilation in Marfan subjects and suggest preservation of basal NO release. Selective loss of flow-mediated dilation suggests a role for fibrillin in endothelial cell mechanotransduction.  (+info)

Adrenoreceptors of the guinea-pig urinary bladder. (5/8871)

1 Adrenaline, noradrenaline and isoprenaline (5 mug/ml) did not affect the resting tone of the isolated urinary bladder of the guinea-pig. 2 The catecholamines (1-2 mug/ml) inhibited neuronally evoked contractions at various stimulation frequencies; the inhibition was maximum at 2 Hz and minimum at 50 Hz. Isoprenaline produced maximum inhibition. 3 Propranolol (0.5 mug/ml) completely blocked the catecholamine-induced inhibition at all the frequencies employed. The concentration-response curves of isoprenaline at 2, 10 and 50 Hz were characteristically shifted by propranolol (50 ng/ml). Phenoxybenzamine (0.2 mug/ml) was totally ineffective. 4 In some experiments adrenaline significantly raised the tone of the bladder exposed to propranolol; this effect could be blocked by phenoxybenzamine. 5 Acetylcholine-induced bladder contractions were inhibited by adrenaline (2 mug/ml); the inhibition was completely blocked by propranolol (0.5 mug/ml). 6 The results indicate the presence of an inhibitory beta-adrenoceptor and suggest the possibility of an excitatory alpha-adrenoceptor in guinea-pig urinary bladder.  (+info)

Calcium responses induced by acetylcholine in submucosal arterioles of the guinea-pig small intestine. (6/8871)

1. Calcium responses induced by brief stimulation with acetylcholine (ACh) were assessed from the fluorescence changes in fura-2 loaded submucosal arterioles of the guinea-pig small intestine. 2. Initially, 1-1.5 h after loading with fura-2 (fresh tissues), ACh increased [Ca2+]i in a concentration-dependent manner. This response diminished with time, and finally disappeared in 2-3 h (old tissues). 3. Ba2+ elevated [Ca2+]i to a similar extent in both fresh and old tissues. ACh further increased the Ba2+-elevated [Ca2+]i in fresh tissues, but reduced it in old tissues. Responses were not affected by either indomethacin or nitroarginine. 4. In fresh mesenteric arteries, mechanical removal of endothelial cells abolished the ACh-induced increase in [Ca2+]i, with no alteration of [Ca2+]i at rest and during elevation with Ba2+. 5. In the presence of indomethacin and nitroarginine, high-K+ solution elevated [Ca2+]i in both fresh and old tissues. Subsequent addition of ACh further increased [Ca2+]i in fresh tissues without changing it in old tissues. 6. Proadifen, an inhibitor of the enzyme cytochrome P450 mono-oxygenase, inhibited the ACh-induced changes in [Ca2+]i in both fresh and Ba2+-stimulated old tissues. It also inhibited the ACh-induced hyperpolarization. 7. In fresh tissues, the ACh-induced Ca2+ response was not changed by apamin, charybdotoxin (CTX), 4-aminopyridine (4-AP) or glibenclamide. In old tissues in which [Ca2+]i had previously been elevated with Ba2+, the ACh-induced Ca2+ response was inhibited by CTX but not by apamin, 4-AP or glibenclamide. 8. It is concluded that in submucosal arterioles, ACh elevates endothelial [Ca2+]i and reduces muscular [Ca2+]i, probably through the hyperpolarization of endothelial or smooth muscle membrane by activating CTX-sensitive K+ channels.  (+info)

Somatostatin induces hyperpolarization in pancreatic islet alpha cells by activating a G protein-gated K+ channel. (7/8871)

Somatostatin inhibits glucagon-secretion from pancreatic alpha cells but its underlying mechanism is unknown. In mouse alpha cells, we found that somatostatin induced prominent hyperpolarization by activating a K+ channel, which was unaffected by tolbutamide but prevented by pre-treating the cells with pertussis toxin. The K+ channel was activated by intracellular GTP (with somatostatin), GTPgammaS or Gbetagamma subunits. It was thus identified as a G protein-gated K+ (K(G)) channel. RT-PCR and immunohistochemical analyses suggested the K(G) channel to be composed of Kir3.2c and Kir3.4. This study identified a novel ionic mechanism involved in somatostatin-inhibition of glucagon-secretion from pancreatic alpha cells.  (+info)

Inhibition of endothelium-dependent hyperpolarization by endothelial prostanoids in guinea-pig coronary artery. (8/8871)

1. In smooth muscle of the circumflex coronary artery of guinea-pig, acetylcholine (ACh, 10(-6) M) produced an endothelium-dependent hyperpolarization consisting of two components. An initial component that occurs in the presence of ACh and a slow component that developed after ACh had been withdrawn. Each component of the hyperpolarization was accompanied by an increase in membrane conductance. 2. Indomethacin (5 x 10(-6) M) or diclofenac (10(-6) M), both inhibitors of cyclooxygenase, abolished only the slow hyperpolarization. The initial hyperpolarization was not inhibited by diclofenac nor by nitroarginine, an inhibitor of nitric oxide synthase. 3. Both components of the ACh-induced hyperpolarization were abolished in the presence of atropine (10(-6) M) or high-K solution ([K+]0 = 29.4 mM). 4. The interval between ACh-stimulation required to generate an initial hyperpolarization of reproducible amplitude was 20 min or greater, but it was reduced to less than 5 min after inhibiting cyclooxygenase activity. Conditioning stimulation of the artery with substance P (10(-7) M) also caused a long duration (about 20 min) inhibition of the ACh-response. 5. The amplitude of the hyperpolarization generated by Y-26763, a K+-channel opener, was reproducible within 10 min after withdrawal of ACh. 6. Exogenously applied prostacyclin (PGI2) hyperpolarized the membrane and reduced membrane resistance in concentrations over 2.8 x 10(-9)M. 7. At concentrations below threshold for hyperpolarization and when no alteration of membrane resistance occurred, PGI2 inhibited the initial component of the ACh-induced hyperpolarization. 8. It is concluded that endothelial prostanoids, possibly PGI2, have an inhibitory action on the release of endothelium-derived hyperpolarizing factor.  (+info)

Effects of PKC activators on ACh-induced increases in [Ca2+]i. Fura-2 loaded endothelial cells were treated with ACh (3 μmol/L) followed by washing. Cells were
This study was designed to determine whether the endothelium-derived relaxing factor induced by acetylcholine (1 microM) in rabbit thoracic aorta inhibits agonist-induced calcium mobilization, specifically calcium influx. Force generated in rings of rabbit thoracic aorta by norepinephrine (1 microM) was measured under isometric conditions. At the appropriate time during 1 microM acetylcholine-induced relaxation of 1 microM norepinephrine-contracted rabbit thoracic aorta, the rings were pulse-labelled with calcium-45 to measure calcium influx. When measured in this fashion, 1 microM acetylcholine decreased the 1 microM norepinephrine-induced increase in calcium influx. This effect was eliminated by removal of the endothelium and by atropine (1 microM), but not by indomethacin (14 microM). Acetylcholine (1 microM) also blocked the 60 mM potassium-chloride-induced increase in calcium influx without dramatically affecting force. The phasic contraction produced by norepinephrine (1 microM) with 2 mM ...
TY - JOUR. T1 - Sodium ion transport participates in non-neuronal acetylcholine release in the renal cortex of anesthetized rabbits. AU - Shimizu, Shuji. AU - Akiyama, Tsuyoshi. AU - Kawada, Toru. AU - Sata, Yusuke. AU - Turner, Michael James. AU - Fukumitsu, Masafumi. AU - Yamamoto, Hiromi. AU - Kamiya, Atsunori. AU - Shishido, Toshiaki. AU - Sugimachi, Masaru. PY - 2017/9. Y1 - 2017/9. N2 - This study examined the mechanism of release of endogenous acetylcholine (ACh) in rabbit renal cortex by applying a microdialysis technique. In anesthetized rabbits, a microdialysis probe was implanted into the renal cortex and perfused with Ringers solution containing high potassium concentration, high sodium concentration, a Na+/K+-ATPase inhibitor (ouabain), or an epithelial Na+ channel blocker (benzamil). Dialysate samples were collected at baseline and during exposure to each agent, and ACh concentrations in the samples were measured by high-performance liquid chromatography. High potassium had no ...
When the acetylcholine levels drop listed below a particular level, it is known as acetylcholine deficiency. As a result of a variety of reasons, acetylcholine deficiency is caused. To find out about your particular problem, the physician has to have a checkup first. The specific therapy relies on lots of factors, like for how much time the client has been experiencing acetylcholine deficiency and also to what degree are the levels of acetylcholine reduced. Relying on just how much acetylcholine deficiency is in your case, you will experience various symptoms. A few of the major signs and symptoms of acetylcholine deficiency include bad listening skills, not having the capacity to focus for longer periods of time, poor development of memory and also recalling as well as the sluggish processing of details. The reason that you experience these signs is that, in all these elements, acetylcholine plays an important duty. Reduced degrees of acetylcholine are caused if you do not get it from different ...
Description of the drug Acetylcholine Chloride. - patient information, description, dosage and directions. What is Acetylcholine Chloride!
View Notes - Physio Review Notes from BIO SCI 94 at University of California, Irvine. Physio Review Notes Nervous System Lecture 1 2 types of neurons: cholinergic: release acetylcholine adregeneric:
The cholinergic hypothesis proposes that Alzheimers disease is caused by insufficient or reduced synthesis of the neurotransmitter acetylcholine. This acetylcholine deficiency hypothesis is not not widely supported because it does not address directly the underlying cause of the disease or the disease progression.. The clinical trials have shown that therapies that support acetylcholine may reduce the symptoms of Alzheimers disease, but do not reverse or stop the disease. Inadequate acetylcholine synthesis is a consequence of generalized brain deterioration observed in Alzheimers disease as well as non-Alzheimers patients. Nevertheless, therapies that support acetylcholine are important to perhaps prevent Alzheimers disease and to maintain proper neurotransmitter balance.. Acetylcholine is the most abundant neurotransmitter in the brain. Acetylcholine is also produced in the Intestines.. According the National Health and Nutrition Examination Survey (NHANES) in 2003-2004, only about 10% of ...
Find right answers right now! If acetylcholine causes excitation of a postsynaptic neuron, to what type of membrane channel did the ACh bind to? More questions about Science & Mathematics, what
Experiments were performed to determine whether acetylcholine affects the sympathetic activation of the cutaneous veins of the dog. Changes in isometric tension of saphenous vein strips were recorded at 37°C in an organ bath. Addition of acetylcholine at 10-11 to 10-8 g/ml did not affect basal tension, but larger doses (5 x 10-8 to 5 x 10-7 g/ml) caused a contraction of the strips which varied from slight to marked. Acetylcholine at 10-8 to 10-7 g/ml caused a further increase in tension when it was added to strips already contracted by norepinephrine, tyramine, KCl, or BaCl2; in contrast, similar doses of acetylcholine caused relaxation of strips contracted by liberation of norepinephrine from the nerve terminals by electrical stimulation (1-10 cps). This relaxation was not influenced by propranolol or hexamethonium but was abolished by atropine (10-8 g/ml). In intact dogs, the lateral saphenous vein was perfused with autologous blood at constant flow. A sustained venoconstriction was induced ...
Learn about Miochol-E (Acetylcholine Chloride Intraocular Solution) may treat, uses, dosage, side effects, drug interactions, warnings, patient labeling, reviews, and related medications.
Ganstigmine (CHF2819) is a novel, orally active acetylcholinesterase inhibitor that induces a stimulation of brain cholinergic transmission. In vivo studies show that, in rat prefrontal cortex, extracellular acetylcholine (ACh) concentrations are significantly increased either after local (1 and 10M) or oral (1.5 and 3 mg/kg) administration. Moreover, repeated oral treatment (six consecutive days; 3 mg/kg) with ganstigmine significantly increases basal extracellular concentrations of ACh in rat prefrontal cortex. Then, acute ganstigmine administration induces a significant increase in extracellular ACh concentrations (actual values) with respect to the last sample in ganstigmine-treated rats. Concentrations of serotonin (5-HT) and noradrenaline (NA) are not affected by any oral dose of ganstigmine (1.5 and 3 mg/kg) used. Moreover, levels of dopamine (DA) and metabolites are not modified either. Basal extracellular concentrations of 5-HT, NA, DA and metabolites are not affected by repeated (six ...
It is well-known that cardiac hypertrophy and arterial and renal dysfunction are serious complications of hypertension. Therefore, we investigated the chronic effects of 606A (2-propyl-3-[2′(1,I,H,/I,-tetrazole-5-yl)biphenyl-4-yl]methyl-5-acetyl-4, 5, 6, 7-tetrahydro imidazo[4, 5-,I,c,/I,]pyridine-4-carboxylic acid disodium salt), a novel AT,SUB,1,/SUB,-receptor antagonist, on these complications of hypertension in stroke-prone spontaneously hypertensive rats (SHRSP) using Wistar Kyoto rats (WKY) as the control. After 8 weeks treatment from 16 weeks of age with 606A by a subcutaneously implanted osmotic pump, cardiac function, cardiac weight, acetylcholine-induced endothelium-dependent relaxation in the isolated aorta and renal function were estimated. Furthermore, wall thickness of the left ventricle was studied morphologically. We found that 606A (0.3 mg, 1 mg and 3 mg/head/day) dose-dependently lowered blood pressure without any effects on heart rate in SHRSP. Long-term treatments with 606A ...
The neurotransmitter acetylcholine is an important modulator of cognitive functions such as learning, memory, and attention. These functions of acetylcholine are mediated by its binding to five distinct subtypes of muscarinic ...
Angiotensin II (Ang II) promotes vascular disease and hypertension in part by the formation of pro-inflammatory cytokines, oxidative stress and inflammation. Signal transducer and activator of transcription 3 (STAT3) is a transcription factor known to play key roles in cytokine signaling and growth in immune cells. We tested the hypothesis that STAT3 plays an essential role in Ang II-induced vascular dysfunction and hypertension. Responses of carotid arteries from C57BL6 mice were examined in vitro after 22-hour incubation with vehicle or Ang II (10 nM) in the presence or absence of a small molecule inhibitor of STAT3 activation, S3I-201. The endothelium-dependent agonist acetylcholine (Ach) produced relaxation in arteries treated with vehicle and the response was inhibited by ~50% by Ang II (P|0.01). S3I-201 (10 πM) co-incubation prevented the Ang II-induced dysfunction. Relaxation to nitroprusside, an endothelium-independent agonist, was not altered in any group. Ang II increased vascular superoxide
Endogenous Acetylcholine Release Enhances Granule Cell Excitability by Lowering the Action Potential Threshold(Ai) Hippocampal slice preparation schematic and e
Renegade immune system. Since the 1970s, its been understood that most MG is due to the immune systems mistaken attack on multiprotein structures called acetylcholine receptors, docking sites on muscle fibers that receive a chemical called acetylcholine from nerve cells. Normally, the presence of acetylcholine causes a muscle fiber to contract, allowing muscle activity to occur.. In most cases of MG, the immune systems inappropriate target is these docking sites. An immune response, in the form of immune system proteins called antibodies, blocks or destroys the acetylcholine receptors, preventing them from receiving the "go" signal from acetylcholine.. In fact, MG is a classic autoimmune disease, a type of disorder in which the body produces an immune response against itself.. These days, its known that the acetylcholine receptors are the most common but not the only target of the immune system in MG. In some people with MG, the target is a protein known as muscle-specific kinase, or MuSK. ...
Acetylcholine is a neurotransmitter that is responsible for gated binding control of cation channels to allow inflow of sodium into muscle cells.
In the present study, the role of reactive oxygen species and the contribution of antioxidant defence in the time course of changes in acetylcholine-stimulated endothelium-dependent and sodium nitroprusside-stimulated endothelium-independent relaxation were investigated in aortic rings isolated from 6-month streptozotocin-diabetic and age-matched control rats. Although there were no significant differences in the degree of the peak relaxations produced by a single administration of acetylcholine (1 μM) or sodium nitroprusside (0.01 μM) between control and diabetic rings, the endothelium-dependent and -independent relaxant responses were more transient and the time required to reach a peak relaxation after addition of acetylcholine was shorter in diabetic vessels. Pretreatment of diabetic vessels with superoxide dismutase (100 U/ml) normalized the recovery phases of endothelium-dependent and -independent relaxations, but had no effect on the peak responses to acetylcholine and sodium ...
Bovine adrenal medullary slices were incubated at 30° in Lockes solution containing orthophosphate-32P or glycerol-1-14C. 32P was incorporated into all individual phospholipids, but at different rates. The highest specific activity observed was in phosphatidylinositol, followed by phosphatidic acid, phosphatidylcholine, phosphatidylserine, lysophosphatidylcholine (lysolecithin), sphingomyelin, and phosphatidylethanolamine.. Acetylcholine (10-5 M)in the presence of eserine (10-5 M) produced a 3-fold increase in catecholamine release and stimulated the incorporation of 32P into phosphatidic acid (3.4-fold), phosphatidylinositol (2.7-fold), and phosphatidylcholine (1.4-fold).. The uptake of orthophosphate-32P into the chromaffin tissue, as well as the specific activities and tissue levels of orthophosphate and nucleotides, were not modified upon acetylcholine stimulation.. Glycerol-1-14C was incorporated into all the individual phospholipids, but, in contrast to 32P incorporation, acetylcholine ...
Animal and human studies have shown that a decrease in acetylcholine may be responsible for some of the cognition deficits in Alzheimers disease.
Oxiracetams mechanisms of action are somewhat similar to other supplements in the racetam family. Although these mechanisms are still not fully understood, it is believe to work by modulating levels of the neurotransmitters acetylcholine and glutamate. Acetylcholine is a vital neurotransmitter that is involved in many functions ranging from neuromuscular control to arousal and reward mechanisms in the central nervous system. When concerning cognitive enhancement, this neurotransmitter is able to contribute to the formation of new memories, while deficits of acetylcholine are commonly associated with memory impairment seen in Alzheimers. Additionally, acetylcholine plays a role in synaptic plasticity which refers to your brains ability to alter synaptic connections between neurons. These connections represent information and memories, so having a higher level of synaptic plasticity will allow for the process of memory formation and learning to be carried out with greater ...
Certain medication may affect your thinking skills; a lessor known and potentially debilitating side affect:. Anticholinergics, which can be found in over-the-counter and prescription medication, can alter your mental status and put older people at a higher risk for falls. Anticholinergics may be found in medications that treat for muscle spasms, depression, incontinence and allergies. Many of these medications are taken by the elderly thereby further increasing their risk for falls and cognitive function.. How does Acetylcholine affect the brain?. These common medications can block acetylcholine, which is a neurotransmitter responsible for stimulation and activity in the brain. Slow brain activity caused by the acetylcholine being blocked, leads to confusion. People who are older tend to take more medication which leads to a chemical reaction that may impact the brain activity and also leaving the brain with higher concentration of acetylcholine. High levels of acetylcholine can eventually ...
Nerve ion channel: 3-D composite electron micrograph of an acetylcholine receptor, a large molecule that controls the transmission of a nerve impulse. Acetylcholine, a neurotransmitter, is released across the junction (synapse) between adjacent nerve cells to bind to receptors on the target cell membrane. A shape change associated with bound neurotransitter/receptor results in pores (ion channels) opening for a fraction of a second. Sodium & potassium ions flood through, altering the electrical potential & firing a second nerve impulse. The ion channel here appears closed. - Stock Image P360/0096
The neurotransmitter acetylcholine (ACh) is bound with 50-micromolar affinity by a completely synthetic receptor (host) comprising primarily aromatic rings. The host provided an overall hydrophobic binding site, but one that could recognize the positive charge of the quaternary ammonium group of ACh through a stabilizing interaction with the electron-rich π systems of the aromatic rings (cation-π interaction). Similar interactions may be involved in biological recognition of ACh and other choline derivatives. ...
TY - JOUR. T1 - Identification of residues in the neuronal α7 acetylcholine receptor that confer selectivity for conotoxin ImI. AU - Quiram, Polly A.. AU - Sine, Steven M.. PY - 1998/5/1. Y1 - 1998/5/1. N2 - To identify residues in the neuronal α7 acetylcholine subunit that confer high affinity for the neuronal-specific toxin conotoxin ImI (CTx ImI), we constructed α7-α1 chimeras containing segments of the muscle α1 subunit inserted into equivalent positions of the neuronal α7 subunit. To achieve high expression in 293 human embryonic kidney cells and formation of homo-oligomers, we joined the extracellular domains of each chimera to the M1 junction of the 5-hydroxytryptamine-3 (5HT-3) subunit. Measurements of CTx ImI binding to the chimeric receptors reveal three pairs of residues in equivalent positions of the primary sequence that confer high affinity of CTx ImI for α7/5HT-3 over α1/5HT-3 homo-oligomers. Two of these pairs, α7Trp55/α1Arg55 and α7Ser59/α1Gln59, are within one of ...
A very important neurotransmitter, acetylcholine is responsible for activating muscles! You wouldnt be able to lift a finger without acetylcholine, so wear it proudly around your neck! This silver-plated necklace features the molecular structure of this important neurotransmitter, finished with a lobster clasp.
Acetylcholine Brain Food™ is designed to promote the production of acetylcholine, a neurotransmitter essential that benefits processing speed.
... Systematic (IUPAC) name 2-acetoxy-N,N,N-trimethylethanaminium Identifiers CAS number 51-84-3 ATC code S01EB09 PubChem 187 DrugBank
Bachem offers H-4186 Acetylcholine Receptor α₁ (129-145) (human, bovine, rat, mouse) for your research. Find all specific details here. Find product specific information including available pack sizes, CAS, detailed description and references here.
... (ACh) is an organic chemical that functions in the brain and body of many types of animals (and humans) as a neurotransmitter-a chemical message released by nerve ce
According to the University of San Diego School of Medicine, "a non-dilated view of the retina is adequate for a general exam in which the patient has no specific ophthalmologic complaints." Had I only known that yesterday I could have avoided hours of distorted vision that made me queasy and gave me a headache. I did have sensitivity to light, albeit minimal, but elected to shut the lights off in my room anyway. That eliminated the sparkling rainbow halos around the lights which were no good to me anyway as my near vision was so blurry I could not possibly read or do sodoku. Thats the real bothersome side effect - and one people should be warned about in advance. If you have to work or be at all productive for the rest of the day youd be up a creek. Watching a movie was pointless too. I was tempted to call it good and go to bed early, but at five, that seemed crazy ...
The study of transmitter interactions in reward and motor pathways in the brain, including the striatum, requires methodology to detect stimulus-driven neurotransmitter release events. Such methods exist for dopamine, and have contributed to the understanding of local and behavioral factors that regulate dop Recent HOT articles In memory of Craig Lunte
There the electrical sign alterations right into a chemical 1, along with the nerve ending sprays a molecular transmitter, acetylcholine, onto the muscle mass. During the milliseconds just before enzymes have an opportunity to chew it up, a lot of the acetylcholine binds with receptors, known as gated-ion channels, within the surface on the muscle mobile. When acetylcholine sticks to them, they open up, making it possible for the sodium ions from the encompassing salty fluid to hurry in ...
AP reaches teminal of MN→ Ca++ influx occurs via volt-gated Ca++ channels → synaptic ACh excytosis (1 vesicle = 10,000 molecules of ACh) → ACh diffuses to junct. folds, binds nicotinic AChR → depolarization (endplate potential) ...
(E)-5-(Pyrimidin-5-yl)-1,2,3,4,7,8-hexahydroazocine (TC299423) is a novel agonist for nicotinic acetylcholine receptors (nAChRs). We examined its efficacy, affinity, and potency for α6β2* (α6β2-containing), α4β2*, and α3β4* nAChRs, using [125I]-epibatidine binding, whole-cell patch-clamp recordings, and synaptosomal 86Rb+ efflux, [3H]-dopamine release, and [3H]-acetylcholine release. TC299423 displayed an EC50 of 30 - 60 nM for α6β2* nAChRs in patch-clamp recordings and [3H]-dopamine release assays. Its potency for α6β2* in these assays was 2.5-fold greater than that for α4β2*, and much greater than that for α3β4*-mediated [3H]-acetylcholine release. We observed no major off-target binding on 70 diverse molecular targets. TC299423 was bioavailable after intraperitoneal or oral administration. Locomotor assays, measured with gain-of-function mutant α6 (α6L9ʹS) nAChR mice, show that TC299423 elicits α6β2* nAChR-mediated responses at low doses. Conditioned place preference (CPP)
Prolyl oligopeptidase (PREP, EC 3.4.21.26) inhibitors have potential as cognition enhancers, but the mechanism of action behind the cognitive effects remains unclear. Since acetylcholine (ACh) and dopamine (DA) are known to be associated with the regulation of cognitive processes, we investigated the effects of two PREP inhibitors on the extracellular levels of ACh and DA in the rat striatum using in vivo microdialysis. KYP-2047 and JTP-4819 were administered either as a single systemic dose (50 μmol/kg∼17 mg/kg i.p.) or directly into the striatum by retrodialysis via the microdialysis probe (12.5, 37.5 or 125 μM at 1.5 μl/min for 60 min). PREP inhibitors had no significant effect on striatal DA levels after systemic administration. JTP-4819 significantly decreased ACh levels both after systemic (by ∼25%) and intrastriatal (by ∼3050%) administration. KYP-2047 decreased ACh levels only after intrastriatal administration by retrodialysis (by ∼4050%) when higher drug levels were reached, ...
Background and purpose: Previous work has shown that NG-monomethyl-l-arginine (l-NMMA) paradoxically inhibits basal, but not ACh-stimulated activity of nitric oxide in rat aorta. The aim of this study was to determine if the endogenously produced agent, asymmetric NG, NG-dimethyl-l-arginine (ADMA), also exhibits this unusual selective blocking action. Experimental approach: The effect of ADMA on basal nitric oxide activity was assessed by examining its ability to enhance phenylephrine (PE)-induced tone in endothelium-containing rings. Its effect on ACh-induced relaxation was assessed both in conditions where ADMA greatly enhanced PE tone and where tone was carefully matched with control tissues at a range of different levels. Key results: ADMA (100 µM) potentiated PE-induced contraction, consistent with inhibition of basal nitric oxide activity. Higher concentrations (300-1000 µM) had no greater effect. Although ADMA (100 µM) also appeared to block ACh-induced relaxation when it enhanced PE ...
METHODS AND RESULTS Rings were examined in myograph systems for isometric tension recording. In untreated WKY and SHR rings, acetylcholine (10(-9) to 10(-5) mol/L) but not bradykinin, substance P (both 10(-6) mol/L), or thrombin (1 U/mL) induced comparable endothelium-dependent relaxations. These relaxations were markedly decreased by NG-monomethyl-L-arginine (10(-4) mol/L) and fully prevented by N omega-nitro-L-arginine methyl ester (10(-4) mol/L) or methylene blue (10(-5) mol/L). In vitro treatment of WKY and SHR rings with benazeprilat, CGP 48369, or valsartan (3 x 10(-7) mol/L) did not affect responses to acetylcholine. In SHR, chronic therapy for 8 weeks with benazepril HCl, CGP 48369, valsartan, or nifedipine (each 10 mg.kg-1.d-1 PO) similarly reduced blood pressure and increased endothelium-dependent relaxations to acetylcholine (log shift at IC50, ie, half-maximal inhibition of a preceding contraction, 10-, 8-, 13-, and 13-fold, P , .05 versus control), whereas relaxations to the NO ...
TY - CHAP. T1 - Impaired acetylcholine synthesis accompanying reduced pyruvate oxidation in rat brain minces. AU - Gibson, G. E.. AU - Jope, Richard S. AU - Blass, J. P.. PY - 1974/12/1. Y1 - 1974/12/1. UR - http://www.scopus.com/inward/record.url?scp=0016230974&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=0016230974&partnerID=8YFLogxK. M3 - Chapter. AN - SCOPUS:0016230974. VL - 5. BT - TRANS.AMER.SOC.NEUROCHEM.. ER - ...
The present study on dilute suspensions of synaptosomes from rat hippocampus yields evidence that feedback regulation of acetylcholine release in this preparation is exerted by a muscarinic autoreceptor localized on the cholinergic nerve ending itself. A possible model for the sequence of events which may take place at the cholinergic nerve ending is presented. Fresh surgical material has been used to demonstrate that the release of acetylcholine in the human cerebral cortex is also regulated by presynaptic muscarinic receptors. An in vitro test system for the study of drugs which affect the release of acetylcholine has been developed. This system was used to examine the effect of a novel cholinergic ligand, N-methyl-N(l-methyl-4-pyrrolidino-2-butynyl) acetamide, on 3 the release of H-acetylcholine. This ligand appears to act as a presynaptic antagonist and a postsynaptic agonist.. ...
Circulating blood generates frictional forces (shear-stress) on the walls of blood vessels. These frictional forces critically regulate vascular function. The endothelium senses these frictional forces and, in response, releases various vasodilators that relax smooth muscle cells in a process termed flow-mediated dilatation. Whilst some elements of the signalling mechanisms have been identified, precisely how flow is sensed and transduced to cause the release of relaxing factors is poorly understood. By imaging signalling in large areas of the endothelium of intact arteries, we show that the endothelium responds to flow by releasing acetylcholine. Once liberated, acetylcholine acts to trigger calcium release from the internal store in endothelial cells, nitric oxide production and artery relaxation. Flow-activated release of acetylcholine from the endothelium is non-vesicular and occurs via organic cation transporters. Acetylcholine is generated following mitochondrial production of acetylCoA. ...
PQ treatment markedly impaired endothelium-dependent relaxations to acetylcholine in PARP-1(-/-), but not PARP-1(+/+) mice (p,0.0001). Maximal relaxation was 45% in PQ treated PARP-1(-/-) mice compared to 79% in PARP-1(+/+) mice. In contrast, endothelium-independent relaxations to sodium nitroprusside (SNP) were not altered. After PQ treatment, l-NAME enhanced contractions to norepinephrine by 2.0-fold in PARP-1(-/-) mice, and those to acetylcholine by 3.3-fold, respectively, as compared to PARP-1(+/+) mice. PEG-superoxide dismutase (SOD) and PEG-catalase prevented the effect of PQ on endothelium-dependent relaxations to acetylcholine in PARP-1(-/-) mice (p,0.001 vs. PQ treated PARP-1(+/+) mice. Indomethacin restored endothelium-dependent relaxations to acetylcholine in PQ treated PARP-1(-/-) mice (p,0.05 vs. PQ treated PARP-1 ...
I went to work today sporting a pair of molecular earrings: serotonin and norepinephrine to be precise. Two non-chemist colleagues spotted them and wondered about the significance of the molecules (and where to get them!). "Serotonin for serenity, norepinephrine for energy." "Ah, youre in balance then!" When I walked past ten minutes later they were browsing the molecular earring site and trying to figure out how to pronounce "acetyl" (as in acetylcholine). The site says that acetylcholine can promote creativity, learning, dreaming and memory. In passing, I noted that many pesticides are acetylcholinesterase inhibitors, they block the breakdown of acetycholine, which can have nasty effects on the body. Which led one colleague to wonder if that was why "suburban cul-de-sacs were such cranky places ...
Decamethonium is used in anesthesia to cause paralysis. It is a short acting depolarizing muscle relaxant. It is similar to acetylcholine and acts as a partial agonist of the nicotinic acetylcholine receptor.
One technique you may utilize to enable you to commit things to memory would be to use Acetylcholine Supplement. A How to Increase Acetylcholine is a simple technique to aid recall of advice youre attempting to remember. You might develop a rhyme, a joke or a joke to help you recall an item of information. Its possible for you to use this same sort of rhyming scheme to allow you to recall period or a specific date ...
Acetylcholine (ACh) is a neurotransmitter widely distributed in the central (and also peripheral, autonomic and enteric) nervous system (CNS). In the CNS, ACh facilitates many functions, such as learning, memory, attention and motor control. When released in the synaptic cleft, ACh binds to two distinct types of receptors: Ionotropic nicotinic acetylcholine receptors (nAChR) and metabotropic muscarinic acetylcholine receptors (mAChRs). The activation of nAChR by ACh leads to the rapid influx of Na+ and Ca2+ and subsequent cellular depolarization. Activation of mAChRs is relatively slow (milliseconds to seconds) and, depending on the subtypes present (M1-M5), they directly alter cellular homeostasis of phospholipase C, inositol trisphosphate, cAMP, and free calcium. In the cleft, ACh may also be hydrolyzed by acetylcholinesterase (AChE) into choline and acetate. The choline derived from ACh hydrolysis is recovered by a presynaptic high-affinity choline transporter (CHT ...
Acetylcholine (ACh) is a neurotransmitter widely distributed in the central (and also peripheral, autonomic and enteric) nervous system (CNS). In the CNS, ACh facilitates many functions, such as learning, memory, attention and motor control. When released in the synaptic cleft, ACh binds to two distinct types of receptors: Ionotropic nicotinic acetylcholine receptors (nAChR) and metabotropic muscarinic acetylcholine receptors (mAChRs). The activation of nAChR by ACh leads to the rapid influx of Na+ and Ca2+ and subsequent cellular depolarization. Activation of mAChRs is relatively slow (milliseconds to seconds) and, depending on the subtypes present (M1-M5), they directly alter cellular homeostasis of phospholipase C, inositol trisphosphate, cAMP, and free calcium. In the cleft, ACh may also be hydrolyzed by acetylcholinesterase (AChE) into choline and acetate. The choline derived from ACh hydrolysis is recovered by a presynaptic high-affinity choline transporter (CHT ...
Acetylcholine (ACh) is a neurotransmitter widely distributed in the central (and also peripheral, autonomic and enteric) nervous system (CNS). In the CNS, ACh facilitates many functions, such as learning, memory, attention and motor control. When released in the synaptic cleft, ACh binds to two distinct types of receptors: Ionotropic nicotinic acetylcholine receptors (nAChR) and metabotropic muscarinic acetylcholine receptors (mAChRs). The activation of nAChR by ACh leads to the rapid influx of Na+ and Ca2+ and subsequent cellular depolarization. Activation of mAChRs is relatively slow (milliseconds to seconds) and, depending on the subtypes present (M1-M5), they directly alter cellular homeostasis of phospholipase C, inositol trisphosphate, cAMP, and free calcium. In the cleft, ACh may also be hydrolyzed by acetylcholinesterase (AChE) into choline and acetate. The choline derived from ACh hydrolysis is recovered by a presynaptic high-affinity choline transporter (CHT ...
Read "Synaptic excitation and inhibition resulting from direct action of acetylcholine on two types of chemoreceptors on individual amphibian parasympathetic neurones, The Journal of Physiology" on DeepDyve, the largest online rental service for scholarly research with thousands of academic publications available at your fingertips.
Vascular endothelial cells respond to certain vasoactive agents by releasing factors which act on medial smooth muscle to cause relaxation or contraction of blood vessels. One of the substances responsible for endothelium-dependent relaxation to acetylcholine has recently been identified as nitric oxide. We have tested the hypothesis that the ability of vascular endothelium to cause relaxation in response to stimulation by vasoactive agents is related in some way to the pattern of perivascular innervation. The actions of acetylcholine and substance P were tested in the presence of methoxamine induced tone in the isolated perfused mesenteric arterial bed of the rat. Tissues were tested from untreated normal 12 week old Sprague-Dawley rats and from rats which had been treated from birth with capsaicin to prevent the development of peptidergic perivascular innervation or 6-hydroxydopamine to prevent development of catecholaminergic innervation. Concentration dependent endothelium-dependent ...
Whaddaya mean 'pure acetylcholine'?[edit]. If there is all this other stuff, B-complex vitamins and whatnot, in royal jelly, ... You can only say, in royal jelly there is also acetylcholine. --Fackel 01:03, 1 June 2006 (UTC) ... how in the heck is the acetylcholine 'pure'? eritain 23:12, 2 December 2005 (UTC) ...
The hemisphere exhibiting SWS is marked by the minimal release of acetylcholine. This model of acetylcholine release has been ... Role of acetylcholine[edit]. Due to the origin of USWS in the brain, neurotransmitters are believed to be involved in its ... The neurotransmitter acetylcholine has been linked to hemispheric activation in northern fur seals. Researchers studied seals ... Unique physiology, including the differential release of the neurotransmitter acetylcholine, has been linked to the phenomenon. ...
See also: Receptor/signaling modulators • Nicotinic acetylcholine receptor modulators • Acetylcholine metabolism/transport ... See also: Receptor/signaling modulators • Muscarinic acetylcholine receptor modulators • Acetylcholine metabolism/transport ... Acetylcholine receptor modulators,state=autocollapse}}. *shows the template collapsed to the title bar if there is a {{navbar}} ... Acetylcholine receptor modulators,state=collapsed}}. to show the template collapsed, i.e., hidden apart from its title bar ...
The protein encoded by this gene synthesizes the neurotransmitter acetylcholine. Acetylcholine acts at two classes of receptors ... The role of acetylcholine at the nicotinic receptor is still under investigation. It is likely implicated in the reward/ ... Choline Acetylcholine It is often used as an immunohistochemical marker for motor neurons (motoneurons). Mutants of ChAT have ... The concentrations of acetylcholine and ChAT are remarkably reduced in the cerebral neocortex and hippocampus. Although the ...
J. Rand (2007). "Acetylcholine". Stephen Gislason (1995). "Neurotransmitter - Serotonin". Brain Mind Center at Alpha Online. R ... Acetylcholine (ACh) is an excitatory, small-molecule neurotransmitter involved in synaptic transmission at neuromuscular ...
Acetylcholine also operates in many regions of the brain, but using different types of receptors, including nicotinic and ... "Acetylcholine Receptors". Ebi.ac.uk. Retrieved 25 August 2014. Schacter, Gilbert and Weger. Psychology.United States of America ... Acetylcholine was the first neurotransmitter discovered in the peripheral and central nervous systems. It activates skeletal ... Nicotine, a compound found in tobacco, is a direct agonist of most nicotinic acetylcholine receptors, mainly located in ...
Neurotransmitter systems: 5-HT: serotonin; DA: dopamine; NE: noradrenalin; ACh: acetylcholine; Glu: glutamate; GH: Growth ... acetylcholine and neuropeptide systems, whereas the three emotionality-related traits emerge as a dysregulation of opioid ... This neurochemical component of the FET hypothesis was upgraded in 2015 by underlying a key role of acetylcholine and ... Differential regulation of fronto-executive function by the monoamines and acetylcholine. Cerebral Cortex 17 (Suppl 1):151-160 ...
Cholinergic neurons-acetylcholine. Acetylcholine is released from presynaptic neurons into the synaptic cleft. It acts as a ... Acetylcholine is synthesized from choline and acetyl coenzyme A. GABAergic neurons-gamma aminobutyric acid. GABA is one of two ... Weakness is typically caused by circulating antibodies that block acetylcholine receptors at the post-synaptic neuromuscular ... motor neurons in the spinal cord that release acetylcholine, and "inhibitory" spinal neurons that release glycine. The ...
High levels of Acetylcholine would thus allow for very rapid learning and remodelling of synaptic connections, with the ... Acetylcholine is proposed to facilitate the balance between memory storage and memory renewal, finding an optimal balance ... Acetylcholine thus modulates plasticity in the Hippocampus, Cerebral Cortex and Striatum to facilitate ideal learning ... Hasselmo, Michael (1993). "Acetylcholine and memory". Trends in Neurosciences. Retrieved 2013-08-04. Doya, K. (2002). " ...
... is a sulfinic acid that is an intermediate in the biosynthesis of taurine. Like taurine, it also acts as an endogenous neurotransmitter via action on the glycine receptors.[1] Hypotaurine is derived from cysteine (and homocysteine). In mammals, the biosynthesis of hypotaurine from cysteine occurs in the pancreas. In the cysteine sulfinic acid pathway, cysteine is first oxidized to its sulfinic acid, catalyzed by the enzyme cysteine dioxygenase. Cysteine sulfinic acid, in turn, is decarboxylated by sulfinoalanine decarboxylase to form hypotaurine. Hypotaurine is enzymatically oxidized to yield taurine by hypotaurine dehydrogenase.[2] ...
Cholinergic system: Acetylcholine. Miscellaneous. *Gasotransmitters: Carbon monoxide (CO). *Hydrogen sulfide (H2S) ...
... (symbol Gly or G;[5] /ˈɡlaɪsiːn/)[6] is an amino acid that has a single hydrogen atom as its side chain. It is the simplest amino acid (since carbamic acid is unstable), with the chemical formula NH2‐CH2‐COOH. Glycine is one of the proteinogenic amino acids. It is encoded by all the codons starting with GG (GGU, GGC, GGA, GGG). Glycine is integral to the formation of alpha-helices in secondary protein structure due to its compact form. For the same reason, it is the most abundant amino acid in collagen triple-helices. Glycine is also an inhibitory neurotransmitter - interference with its release within the spinal cord (such as during a Clostridium tetani infection) can cause spastic paralysis due to uninhibited muscle contraction. Glycine is a colorless, sweet-tasting crystalline solid. It is the only achiral proteinogenic amino acid. It can fit into hydrophilic or hydrophobic environments, due to its minimal side chain of only one hydrogen atom. The acyl radical is glycyl. ...
Acetylcholine: Acetylcholine metabolism and transport modulators. *Muscarinic acetylcholine receptor modulators. *Nicotinic ...
Cholinergic system: Acetylcholine. Miscellaneous. *Gasotransmitters: Carbon monoxide (CO). *Hydrogen sulfide (H2S) ...
Cholinergic system: Acetylcholine. Miscellaneous. *Gasotransmitters: Carbon monoxide (CO). *Hydrogen sulfide (H2S) ...
Small: Acetylcholine. Acetylcholine. Ach. Muscarinic acetylcholine receptors. Nicotinic acetylcholine receptors. Small: ... Acetylcholine system. [24][26][27][28][37]. Cholinergic pathways: Forebrain cholinergic nuclei (FCN):. Nucleus basalis of ... "Acetylcholine Receptors". Ebi.ac.uk. Retrieved 25 August 2014.. *^ Schacter, Gilbert and Weger. Psychology.United States of ... Others: acetylcholine (ACh), anandamide, etc.. In addition, over 50 neuroactive peptides have been found, and new ones are ...
Brain acetylcholine and animal electrophysiology. In: Brain Acetylcholine and Neuropsychiatric Disease, K. L. Davis and P. A. ... Brain acetylcholine and seizures. In: Psychobiology of Convulsive Therapy, M. Fink, S. Kety, J. McGaugh and T. A. Willimas, Eds ... of the United States National Academy of Sciences and he is recipient of a Festschrift on neurobiology of acetylcholine, 1985. ...
ARIA plays a role in synapse development, influencing the upregulation of acetylcholine receptor genes beneath the endplate ... Included in the family are heregulin; neu differentiation factor; acetylcholine receptor synthesis stimulator; glial growth ... or acetylcholine receptor inducing activity (ARIA) Type II NRG1; alternative name: Glial Growth Factor-2 (GGF2); Type III NRG1 ... after mammalian motor neurons have made synaptic contact with muscle fibres, hence its name ARIA = Acetylcholine Receptor ...
"Nicotinic acetylcholine receptors" (PDF). www.ucl.ac.uk/. University College London. Retrieved 4 March 2015. ... The net effect of innervated M3 receptors on blood vessels is vasodilation, as acetylcholine causes endothelial cells to ... The parasympathetic nervous system uses chiefly acetylcholine (ACh) as its neurotransmitter, although peptides (such as ...
Acetylcholine released by preganglionic sympathetic fibers of these nerves acts on nicotinic acetylcholine receptors, causing ... Nicotine acts as an agonist at most nicotinic acetylcholine receptors (nAChRs), except at two nicotinic receptor subunits ( ... By binding to nicotinic acetylcholine receptors in the brain, nicotine elicits its psychoactive effects and increases the ... Additionally, specific types of nicotinic acetylcholine receptors- eg, alpha 7 receptors, which are stimulated by nicotine-are ...
336-337). Phantasmidine is a nicotinic agonist that acts at acetylcholine receptors. It mimics the effects of acetylcholine on ... This influx of positive charge induces the release of acetylcholine into the body to interact with the parasympathetic nervous ... Phantasmidine is characterized in the same class as epibatidine, which is a similar nicotinic acetylcholine agonist derived ... Phantasmidine is selective for nicotinic acetylcholine receptors (nAChR) containing ß4 subunits; however, responses in ...
Gamma-aminobutyric acid receptor subunit alpha-4 is a protein that in humans is encoded by the GABRA4 gene.[5][6] GABA is the major inhibitory neurotransmitter in the mammalian brain where it acts at GABA-A receptors, which are ligand-gated chloride channels. Chloride conductance of these channels can be modulated by agents such as benzodiazepines that bind to the GABA-A receptor. At least 16 distinct subunits of GABA-A receptors have been identified.[6] ...
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Each AMPAR has four sites to which an agonist (such as glutamate) can bind, one for each subunit.[5] The binding site is believed to be formed by the N-terminal tail and the extracellular loop between transmembrane domains three and four.[16] When an agonist binds, these two loops move towards each other, opening the pore. The channel opens when two sites are occupied,[17] and increases its current as more binding sites are occupied.[18] Once open, the channel may undergo rapid desensitization, stopping the current. The mechanism of desensitization is believed to be due to a small change in angle of one of the parts of the binding site, closing the pore.[19] AMPARs open and close quickly (1ms), and are thus responsible for most of the fast excitatory synaptic transmission in the central nervous system.[17] The AMPAR's permeability to calcium and other cations, such as sodium and potassium, is governed by the GluA2 subunit. If an AMPAR lacks a GluA2 subunit, then it will be permeable to sodium, ...
See also: Receptor/signaling modulators • Nicotinic acetylcholine receptor modulators • Acetylcholine metabolism/transport ... See also: Receptor/signaling modulators • Muscarinic acetylcholine receptor modulators • Acetylcholine metabolism/transport ... Acetylcholine synthesis: *Acetyl-CoA is also an important component in the biogenic synthesis of the neurotransmitter ... Choline, in combination with acetyl-CoA, is catalyzed by the enzyme choline acetyltransferase to produce acetylcholine and ...
The neurotransmitter acetylcholine is synthesized by choline acetyltransferase (ChAT) and transported into synaptic vesicles by ... N2 - The neurotransmitter acetylcholine is synthesized by choline acetyltransferase (ChAT) and transported into synaptic ... AB - The neurotransmitter acetylcholine is synthesized by choline acetyltransferase (ChAT) and transported into synaptic ... abstract = "The neurotransmitter acetylcholine is synthesized by choline acetyltransferase (ChAT) and transported into synaptic ...
The nicotinic acetylcholine receptor (nAChR) of Torpedo electric rays has been extensively characterized over the last three ... Biophysical and ion channel functional characterization of the Torpedo californica nicotinic acetylcholine receptor in varying ...
After acetylcholine is released from the nerve terminal, it binds to acetylcholine receptor for a brief period; when it is ... DEFECTS IN ACETYLCHOLINE RECEPTOR (AChR). Primary AChR Deficiency. The acetylcholine receptor is made up 5 subunits. Subunits ... The endplate acetylcholine receptor deficiency is milder than in primary acetylcholine receptor deficiency42 and the junctional ... This medication increases the lifetime of acetylcholine in the synaptic space which allows each acetylcholine molecule to bind ...
... regulates production of antibodies to the acetylcholine receptor and that removing the thymus reduced symptoms. Acetylcholine ... Patients were selected for the study if they had the disease for fewer than five years, elevated levels of acetylcholine ... About 80 percent of patients have elevated levels of antibodies against acetylcholine receptors, proteins on the muscle used to ... Often patients are initially treated with acetylcholinesterase inhibitors, drugs that elevate acetylcholine levels. If that ...
Ultrastucture evidence for acetylcholine receptor dysfunction in myasthenia gravis and its autoimmune model. In: Rowland LM. ... Anti-acetylcholine receptor antibodies in myasthenia gravis: clinical and serological follow-up of individual patients. J ... Influence of alpha-fetoprotein in vitro and in vivo immune responses to acetylcholine receptor. Ann N Y Acad Sci 1981; 377: 208 ... Besinger UA, Toyka KV, Heininger K. Long-term correlation of clinical course and acetylcholine receptor antibody in patients ...
This drug raises the levels of acetylcholine in your dogs brain, and can help to increase muscle strength and motor function. ... Congenital myasthenia gravis is hereditary, and occurs when a dog is born without the appropriate number of acetylcholine ... When canine myasthenia gravis occurs, the number of nerve receptors for acetylcholine in your dogs brain diminishes, leaving ... In a normal dogs nervous system, the nerve endings secrete the neurotransmitter known as acetylcholine, which carries messages ...
See also: Receptor/signaling modulators • Nicotinic acetylcholine receptor modulators • Acetylcholine metabolism/transport ... See also: Receptor/signaling modulators • Muscarinic acetylcholine receptor modulators • Acetylcholine metabolism/transport ... Acetylcholine receptor modulators,state=autocollapse}}. *shows the template collapsed to the title bar if there is a {{navbar}} ... Acetylcholine receptor modulators,state=collapsed}}. to show the template collapsed, i.e., hidden apart from its title bar ...
Media in category "Acetylcholine receptor". The following 16 files are in this category, out of 16 total. ... Receptor de acetilcolina (es); receptor dacetilcolina (ca); Acetylcholinrezeptoren (de); Acetylcholine receptor (en-gb); ... Acetylcholine receptor (en-ca); acetylcholinový receptor (cs); Recettore colinergico (it); récepteur cholinergique (fr); ... acetylcholine receptor (en); مستقبل الأستيل كولين (ar); Υποδοχέας ακετυλοχολίνης (el); Ацетилхолински рецептор (mk) ...
Acetylcholine is a compound produced naturally by the bodys nervous system. ... Miochol-E solution for intraocular use contains the active ingredient acetylcholine. ... Miochol-E (acetylcholine). Miochol-E solution for intraocular use contains the active ingredient acetylcholine. Acetylcholine ... Acetylcholine is a compound produced naturally by the bodys nervous system.. When applied to the eye, acetylcholine stimulates ...
acetylcholine (Ach). Source:. The Oxford Companion to the Mind. Author(s):. Richard L. Gregory. An important neurotransmitter, ...
Acetylcholine receptor antibody is a protein found in the blood of many people with myasthenia gravis. The antibody affects a ... Acetylcholine receptor antibody is a protein found in the blood of many people with myasthenia gravis. The antibody affects a ... An abnormal result means acetylcholine receptor antibody has been found in your blood. It confirms the diagnosis of myasthenia ... Normally, there is no acetylcholine receptor antibody (or less than 0.05 nmol/L) in the bloodstream. ...
ACETYLCHOLINE THERAPY IN EPILEPSY. Br Med J 1933; 1 doi: https://doi.org/10.1136/bmj.1.3779.999 (Published 10 June 1933) Cite ...
Synaptic Release of Acetylcholine Rapidly Suppresses Cortical Activity by Recruiting Muscarinic Receptors in Layer 4 Rajan ...
AChR antibodies are autoantibodies that mistakenly target proteins called acetylcholine receptors that are located on skeletal ... An acetylcholine receptor (AChR) antibody test is used to help diagnose myasthenia gravis (MG), an autoimmune disease that ... Acetylcholine receptors function as "docking stations" for acetylcholine, a chemical substance (neurotransmitter) that ... where it stimulates the release of acetylcholine. Acetylcholine travels across a microscopic gap between the nerve ending and a ...
Acetylcholine definition is - a neurotransmitter [C7H16NO2]+ released at autonomic synapses and neuromuscular junctions and ... Share acetylcholine Post the Definition of acetylcholine to Facebook Share the Definition of acetylcholine on Twitter ... Britannica.com: Encyclopedia article about acetylcholine. Comments on acetylcholine What made you want to look up acetylcholine ... Examples of acetylcholine in a Sentence. Recent Examples on the Web This ends up leaving more acetylcholine intact, Dr. Tan ...
Acetylcholine is now used by bacteria, fungi, and a variety of other animals. Interestingly, many of the uses of acetylcholine ... Nicotine binds to and activates nicotinic acetylcholine receptors, mimicking the effect of acetylcholine at these receptors. ... Substances that interfere with acetylcholine activity are called anticholinergics. Acetylcholine is the neurotransmitter used ... and allow for acetylcholine to dynamically regulate physiological processes. Acetylcholine is synthesized in certain neurons by ...
Muscarinic acetylcholine receptor family (IPR000995) *Muscarinic acetylcholine receptor M1 (IPR002228). *Muscarinic ... Classification of muscarinic acetylcholine receptors.. Pharmacol. Rev. 50 279-90 1998. Bonner TI. The molecular basis of ... Classification of muscarinic acetylcholine receptors.. Pharmacol. Rev. 50 279-90 1998. Wess J. Molecular biology of muscarinic ... Muscarinic acetylcholine receptors: mutant mice provide new insights for drug development.. Nat Rev Drug Discov 6 721-33 2007 ...
InterPro provides functional analysis of proteins by classifying them into families and predicting domains and important sites. We combine protein signatures from a number of member databases into a single searchable resource, capitalising on their individual strengths to produce a powerful integrated database and diagnostic tool.
The acetylcholine nicotinic receptor is an ionic channel whose aperture is directly controlled by acetylcholine. It is a key ... The acetylcholine nicotinic receptor is an ionic channel whose aperture is directly controlled by acetylcholine. It is a key ... Regulation of Neuronal Acetylcholine Receptors by Cell-Cell Interactions Darwin K. Berg, R. Thomas Boyd, Stanley W. Halvorsen, ... Nicotinic Acetylcholine Receptors in Insect Ganglia and Mammalian Brain: Some Comparisons David R. E. Macallan, Susan Wonnacott ...
The muscarinic acetylcholine receptor was functionally defined, based on the actions of specific drugs on specific cells or ... The muscarinic acetylcholine receptor was functionally defined, based on the actions of specific drugs on specific cells or ... Haga, T., Molecular size of muscarinic acetylcholine receptors of rat brain, FEBS Lett. 113, 68-72 (1980).CrossRefGoogle ... Nathanson, N.M., Molecular properties of the muscarinic acetylcholine receptor, Ann. Rev. Neurosci. 10, 195-236 (1987).CrossRef ...
I havent been to the dr yet but do have a copy of my results. I dont know how to read it. it says 0.3 binding, blocking 0., and modulating ab 15% does everybody...
An acetylcholine receptor (abbreviated AChR) is an integral membrane protein that responds to the binding of acetylcholine, a ... Although all acetylcholine receptors, by definition, respond to acetylcholine, they respond to other molecules as well. ... Acetylcholine receptor: PMAP The Proteolysis Map-animation Acetylcholine Receptors at the US National Library of Medicine ... Nicotinic acetylcholine receptors (nAChR, also known as "ionotropic" acetylcholine receptors) are particularly responsive to ...
Help us teach kids of all ages how to prevent traumatic brain and spinal cord injuries! The ThinkFirst Foundation is a 501c3 nonprofit organization. Donate ...
Acetylcholine. Acetylcholine (ACh) is an organic chemical that functions in the brain and body of many types of animals, ... Acetylcholine is now used by bacteria, fungi, and a variety of other animals. Interestingly, many of the uses of acetylcholine ... 3) Acetylcholine is released into the synaptic cleft. (4) Acetylcholine binds to postsynaptic receptors. (5) This binding ... Acetylcholine processing in a synapse. After release acetylcholine is broken down by the enzyme acetylcholinesterase. ...
Alleged Effect of Acetylcholine on Immobilized Joints Br Med J 1938; 1 :835 ... Alleged Effect of Acetylcholine on Immobilized Joints. Br Med J 1938; 1 doi: https://doi.org/10.1136/bmj.1.4032.835 (Published ...
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