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.
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.
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.
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.
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.
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 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.
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.
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.
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.
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)
An alkaloid, originally from Atropa belladonna, but found in other plants, mainly SOLANACEAE. Hyoscyamine is the 3(S)-endo isomer of atropine.
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.
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.
The synapse between a neuron and a muscle.
A slowly hydrolyzed CHOLINERGIC AGONIST that acts at both MUSCARINIC RECEPTORS and NICOTINIC RECEPTORS.
A neuromuscular blocker and active ingredient in CURARE; plant based alkaloid of Menispermaceae.
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.
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.
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.
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.
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.
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.
The physiological widening of BLOOD VESSELS by relaxing the underlying VASCULAR SMOOTH MUSCLE.
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.
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.
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)
Drugs used to cause dilation of the blood vessels.
A subclass of muscarinic receptor that mediates cholinergic-induced contraction in a variety of SMOOTH MUSCLES.
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.
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.
Contractile tissue that produces movement in animals.
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.
An enzyme that catalyzes the formation of acetylcholine from acetyl-CoA and choline. EC 2.3.1.6.
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.
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.
The relationship between the dose of an administered drug and the response of the organism to the drug.
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)
Drugs that bind to and activate cholinergic receptors.
Agents that inhibit the actions of the parasympathetic nervous system. The major group of drugs used therapeutically for this purpose is the MUSCARINIC ANTAGONISTS.
A non-hydrolyzed muscarinic agonist used as a research tool.
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.
A common name used for the genus Cavia. The most common species is Cavia porcellus which is the domesticated guinea pig used for pets and biomedical research.
The 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.
Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.
A high-affinity muscarinic antagonist commonly used as a tool in animal and tissue studies.
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.
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).
Nerve fibers liberating acetylcholine at the synapse after an impulse.
Compounds containing the hexamethylenebis(trimethylammonium) cation. Members of this group frequently act as antihypertensive agents and selective ganglionic blocking agents.
A process leading to shortening and/or development of tension in muscle tissue. Muscle contraction occurs by a sliding filament mechanism whereby actin filaments slide inward among the myosin filaments.
A muscarinic antagonist used to study binding characteristics of muscarinic cholinergic receptors.
Use of electric potential or currents to elicit biological responses.
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 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.
Drugs that bind to but do not activate CHOLINERGIC RECEPTORS, thereby blocking the actions of ACETYLCHOLINE or cholinergic agonists.
The resection or removal of the innervation of a muscle or muscle tissue.
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)
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.
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.
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.
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.
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)
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)
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.
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.
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.
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.
Compounds that contain the decamethylenebis(trimethyl)ammonium radical. These compounds frequently act as neuromuscular depolarizing agents.
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.
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.
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.
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.
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.
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.
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.
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.
The distal and narrowest portion of the SMALL INTESTINE, between the JEJUNUM and the ILEOCECAL VALVE of the LARGE INTESTINE.
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.
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.
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.
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.
That phase of a muscle twitch during which a muscle returns to a resting position.
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.
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.
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)
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.
The rate dynamics in chemical or physical systems.
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.
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 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.
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.
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.
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.
A family of hexahydropyridines.
Endogenously-synthesized compounds that influence biological processes not otherwise classified under ENZYMES; HORMONES or HORMONE ANTAGONISTS.
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).
Part of the arm in humans and primates extending from the ELBOW to the WRIST.
Compounds with a six membered aromatic ring containing NITROGEN. The saturated version is PIPERIDINES.
Chemically stimulated aggregation of cell surface receptors, which potentiates the action of the effector cell.
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.
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.
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.
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.
A competitive inhibitor of nitric oxide synthetase.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
Elements of limited time intervals, contributing to particular results or situations.
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.
Abrupt changes in the membrane potential that sweep along the CELL MEMBRANE of excitable cells in response to excitation stimuli.
The physiological narrowing of BLOOD VESSELS by contraction of the VASCULAR SMOOTH MUSCLE.
Neurons whose primary neurotransmitter is ACETYLCHOLINE.
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)
A group of compounds that are derivatives of beta-methylacetylcholine (methacholine).
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.
Drugs used to cause constriction of the blood vessels.
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.
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.
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.
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.
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.
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.
The parts of a macromolecule that directly participate in its specific combination with another molecule.
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.
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.
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.
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)
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.
An aquatic genus of the family, Pipidae, occurring in Africa and distinguished by having black horny claws on three inner hind toes.
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.
Limbless REPTILES of the suborder Serpentes.
The cartilaginous and membranous tube descending from the larynx and branching into the right and left main bronchi.
A piperidine botanical insecticide.
The part of CENTRAL NERVOUS SYSTEM that is contained within the skull (CRANIUM). Arising from the NEURAL TUBE, the embryonic brain is comprised of three major parts including PROSENCEPHALON (the forebrain); MESENCEPHALON (the midbrain); and RHOMBENCEPHALON (the hindbrain). The developed brain consists of CEREBRUM; CEREBELLUM; and other structures in the BRAIN STEM.
A volatile vasodilator which relieves ANGINA PECTORIS by stimulating GUANYLATE CYCLASE and lowering cytosolic calcium. It is also sometimes used for TOCOLYSIS and explosives.
Arteries which arise from the abdominal aorta and distribute to most of the intestines.
An inhibitor of drug metabolism and CYTOCHROME P-450 ENZYME SYSTEM activity.
The neural systems which act on VASCULAR SMOOTH MUSCLE to control blood vessel diameter. The major neural control is through the sympathetic nervous system.
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).
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.
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.
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)
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)
The lipid- and protein-containing, selectively permeable membrane that surrounds the cytoplasm in prokaryotic and eukaryotic cells.
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)
An NADPH-dependent enzyme that catalyzes the conversion of L-ARGININE and OXYGEN to produce CITRULLINE and NITRIC OXIDE.
An organophosphate cholinesterase inhibitor that is used as a pesticide.
The portion of the descending aorta proceeding from the arch of the aorta and extending to the DIAPHRAGM, eventually connecting to the ABDOMINAL AORTA.
Quantitative determination of receptor (binding) proteins in body fluids or tissue using radioactively labeled binding reagents (e.g., antibodies, intracellular receptors, plasma binders).
A non-selective inhibitor of nitric oxide synthase. It has been used experimentally to induce hypertension.
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.
An essential amino acid that is physiologically active in the L-form.
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.
The action of a drug that may affect the activity, metabolism, or toxicity of another drug.
Established cell cultures that have the potential to propagate indefinitely.
An alpha-1 adrenergic agonist used as a mydriatic, nasal decongestant, and cardiotonic agent.
The veins and arteries of the HEART.
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.
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.
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.
The ability of a substrate to allow the passage of ELECTRONS.
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.
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)
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
The flow of BLOOD through or around an organ or region of the body.
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.
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.
The nonstriated involuntary muscle tissue of blood vessels.
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.
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.
The smallest divisions of the arteries located between the muscular arteries and the capillaries.
Sweat-producing structures that are embedded in the DERMIS. Each gland consists of a single tube, a coiled body, and a superficial duct.
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.
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.
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)
Spasm of the large- or medium-sized coronary arteries.
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.
Compounds containing the PhCH= radical.
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.
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.
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.
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.
A general class of ortho-dihydroxyphenylalkylamines derived from tyrosine.
The most common inhibitory neurotransmitter in the central nervous system.
A group of cold-blooded, aquatic vertebrates having gills, fins, a cartilaginous or bony endoskeleton, and elongated bodies covered with scales.
Neurons which activate MUSCLE CELLS.
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.
A slowly hydrolyzed muscarinic agonist with no nicotinic effects. Pilocarpine is used as a miotic and in the treatment of glaucoma.
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.
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.
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.
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).
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.
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.
PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.
An acridine derivative formerly widely used as an antimalarial but superseded by chloroquine in recent years. It has also been used as an anthelmintic and in the treatment of giardiasis and malignant effusions. It is used in cell biological experiments as an inhibitor of phospholipase A2.

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 ...
After the impulse is transmitted across the synapse, the acetylcholine is broken down by the enzyme cholinesterase. 83+ Ways to Increase or Decrease Acetylcholine. Choline is a precursor for acetylcholine, an important neurotransmitter synthesized by cholinergic neurons and involved in muscle control, circadian rhythm, memory, and many other neuronal functions. Acetylcholine (ACh) is a neurotransmitter that has been receiving a lot of attention in memory research. It is the main neurotransmitter released into the nerves throughout your body (excluding your spinal cord and brain), and is responsible for … While your liver makes choline, it doesnt make enough to meet your daily needs so its … If youre trying to make more acetylcholine, you have to increase your choline levels. These compounds are toxic because they inhibit the action of acetylcholinesterase, leading to a build-up of acetylcholine. Acetylcholine, a biochemical, plays a large role in maintaining your hearts rhythm when you ...
Learn about Miochol-E (Acetylcholine Chloride Intraocular Solution) may treat, uses, dosage, side effects, drug interactions, warnings, patient labeling, reviews, and related medications.
What does acetylcholine do in asthma? As a central messenger of this response, acetylcholine counteracts fight-or-flight … Your brain uses it to transmit, process, and modulate information during cognitive processing, and naturally, thats led to investigation into the use of acetylcholine as a nootropic supplement to improve cognitive function. Too much acetylcholine has been implicated in hives. What inhibits the rise of Acetylcholine in the frontal lobes? flashcard set{{course.flashcardSetCoun > 1 ? Check with your pharmacist. Cest le seul neurotransmetteur utilisé dans le système nerveux somatique et lun des nombreux neurotransmetteurs du système nerveux autonome (SNA). This medicine may interact with other drugs or health problems. It is the target of many of the deadliest neurotoxins. acetylcholine (ACh) [as″ĕ-til-ko´lēn] the acetic acid ester of choline, normally present in many parts of the body and having important physiologic functions. What neurotransmitter decreases ...
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.
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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.
Huperzine A 200mcg (Third Party Tested) Made in The USA, 120 Tablets, Nootropics Brain Supplement to Promote Acetylcholine, Support Memory and Focus by Double Wood Supplements: Amazon.com.au: Health & Personal Care It comes as no surprise, then, that unbalanced brain chemicals can have a far-ranging negative impact on many different cognitive functions. It works as an antioxidant that protects brain cells and also oxidation from environmental toxins. Like Dopamine, acetylcholine is found in collections of cells in specific areas of the brain from where it is sent to nearly every part of the brain. A high-fat diet is known to negatively affect the liver. In a market where effectiveness is often second to unscrupulous marketing, itâ s â ¦ Acetylcholine. â Coffee fruit extract isnâ t just a natural source of caffeineâ itâ s shown to increase BDNF, which is known to help produce new brain cells and strengthen existing ones. It may raise energy levels, create healthy nerve cells, and reduce ...
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.
Acetylcholine Acetylcholine 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.
Acetylcholine (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) ...
receptors for the neurotransmitter acetylcholine implicated in recent research as having an important role in modulating the plaques and tangles characteristic of Alzheimers.. ...
(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)
TY - JOUR. T1 - Patterns of brain acetylcholine release predict individual differences in preferred learning strategies in rats. AU - McIntyre, Christa K.. AU - Marriott, Lisa K.. AU - Gold, Paul E.. PY - 2003/3/1. Y1 - 2003/3/1. N2 - Acetylcholine release was measured simultaneously in the hippocampus and dorsal striatum of rats before and during training on a maze that could be learned using either a hippocampus-dependent spatial strategy or a dorsal striatum-dependent turning strategy. A probe trial administered after rats reached a criterion of 9/10 correct responses revealed that about half of the rats used a spatial strategy and half a turning strategy to solve the task. Acetylcholine release in the hippocampus, as well as the ratio of acetylcholine release in the hippocampus vs. the dorsal striatum, measured either before or during training, predicted these individual differences in strategy selection during learning. These findings suggest that differences in release of acetylcholine ...
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 ...
We contrast the phenotypes associated with hereditary acetylcholine receptor deficiency arising from mutations in either the acetylcholine receptor epsilon subunit or the endplate acetylcholine receptor clustering protein rapsyn. Mutational screening was performed by amplification of promoter and co …
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.
Transient receptor potential canonical type 3 (TRPC3) stations are nonselective cation stations and regulate intracellular Ca2+ focus. and KO mice. Phenylephrine-induced vasoconstriction was low in TRPC3 KO mice in comparison with that of WT mice but neither high K+- nor pressure-induced vasoconstriction was modified in TRPC3 KO mice. Acetylcholine-induced vasorelaxation was inhibited in TRPC3 KO mice and by the selective TRPC3 blocker pyrazole-3. Acetylcholine clogged the phenylephrine-induced upsurge in Ca2+ percentage and then rest in TRPC3 WT mice but got little influence on those results in KO mice. Acetylcholine evoked a Ca2+ upsurge in endothelial cells that was inhibited by pyrazole-3. Acetylcholine induced improved NO launch in TRPC3 WT mice however not in KO mice. Acetylcholine also improved the nitrate/nitrite Brefeldin A focus in TRPC3 WT mice however not in KO mice. Todays research directly demonstrated how the TRPC3 channel can be involved with agonist-induced vasoconstriction and ...
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 ...
Overview on acetylcholine receptors pharmacology: differences between muscarinic and nicotinic receptors, classification, location, acetylcholine receptors and
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This study aimed to examine the effects of aerobic training on endothelium-dependent vasorelaxation induced by acetylcholine and the expression of enzymes controlling NO bioavailability in the aorta of hypertensive rats.. We confirmed findings from previous reports showing that compared with the WKYsd group, the SHRsd group exhibits higher BP and impaired maximal vasorelaxation 24,25. Moreover, the relative endothelium-dependent vasorelaxation induced by 10-4 M ACh was lower in the SHRsd group than in WKY and showed paradoxical vasoconstriction in SHR. These results clearly reveal endothelial dysfunction in the aorta of SHR 24,32. Acetylcholine activates smooth muscle muscarinic receptors and evokes endothelium-dependent contractions in the aortas of SHR, but not WKY 33.. When aorta samples were incubated with L-NAME, differences in maximal vasorelaxation were not observed, but the relative endothelium-dependent vasorelaxation induced by ACh (10-4 M) remained different between the SHRsd and ...
ECHA compiled an inventory of substances likely to meet the criteria of Annex III to the REACH Regulation. The aim is to support registrants in identifying whether reduced minimum information requirements or a full Annex VII information set is required.. The inventory was produced using publicly available databases with experimental data and by using (Q)SAR model results. Indications for hazardous toxicological or ecotoxicological properties together with information on uses and other available relevant information have to be compared with the criteria in Annex III.. The fact that a substance is not in this list does not necessarily mean that the criteria for Annex III are not met. Likewise, if a substance is on this inventory, a registrant can still benefit from the reduced information requirements if it is justified.. Note that the inventory is not a tool for classification, it only shows indications for concern. For instance, the fact that a substance is indicated as Suspected mutagen does ...
Vesicular Acetylcholine Transporter羊多克隆抗体可与大鼠, 豚鼠样本反应并经WB, IHC实验严格验证,被1篇文献引用。所有产品均提供质保服务,中国75%以上现货。
Intrathecally administered cholinergic agonists such as oxotremorine (muscarinic), carbachol (mixed nicotinic and muscarinic agonist), and epibatidine (nicotinic) have all been shown to reduce nociception in behavioral studies. Thus, there is substantial evidence for a role of acetylcholine (ACh) in the control of nociception in the spinal cord, but the mechanisms regulating ACh release are not known. The present study was initiated to establish a rat model to study which mechanisms are involved in the control of ACh release. Spinal microdialysis probes were inserted intraspinally at the C1-C5 spinal level in isoflurane-anesthetized rats. The probes were perfused with Ringers solution containing 10 μM neostigmine to prevent degradation of ACh. Oxotremorine, carbachol, epibatidine, and scopolamine, dissolved in Ringers solution, were administered intraspinally via dialysis and 30 μl/10-min samples of dialysate were collected for HPLC analysis of ACh content. The release of ACh was found to be ...
Sominex is a medication that is also known as an antihistamine. Diphenhydramine is the ingredient that is responsible for the main effects of Sominex.. Uses. Sominex can be used to treat any problems certain individuals may face when trying to sleep. It may be used as a form of treatment for those with insomnia. The components of Sominex work by acting on the neurotransmitters in the brain. The two specific neurotransmitters that are affected by Sominex are histamine and acetylcholine. It is assumed that acetylcholine manages the functions of the brain that are responsible for sleep. It is also supposed that acetylcholine is in charge of alertness. When the actions of histamine and acetylcholine are repressed, individuals begin to feel drowsy. They also find it easier to fall asleep faster.. Sominex can also have other beneficial effects. You should seek the advice of a healthcare expert to determine what these advantages may be.. Dosage. Most medications are only safe when they are taken in ...
Enteric neurons secrete an intimidating array of neurotransmitters. One major neurotransmitter produced by enteric neurons is acetylcholine. In general, neurons that secrete acetylcholine are excitatory, stimulating smooth muscle contraction, increases in intestinal secretions, release of enteric hormones and dilation of blood vessels. Norepinephrine is also used extensively for neurotransmission in the gastrointestinal tract, but it derives from extrinsic sympathetic neurons; the effect of norepinephrine is almost always inhibitory and opposite that of acetylcholine. The enteric nervous system can and does function autonomously, but normal digestive function requires communication links between this intrinsic system and the central nervous system. These links take the form of parasympathetic and sympathetic fibers that connect either the central and enteric nervous systems or connect the central nervous system directly with the digestive tract. Through these cross connections, the gut can ...
Nerve ion channel: Contour map (from electron micrograph data) 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 neurotransmitter/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 (centre) appears closed. - Stock Image P360/0097
In this study, we uncovered a new mechanism that inactivates nAChRs on neurons. We show that relatively mild shifts in the intracellular thiol/disulfide redox state toward more oxidative conditions induce a rundown of ACh-evoked currents. Once the ACh-evoked currents run down, they do not recover for at least 1 h; it is as if the receptors become trapped in a long-lasting inactivated state. This ROS-induced rundown of ACh-evoked currents is specific to neuronal nAChRs, because elevating ROS had no detectable effect on muscle nAChRs.. In previous work (De Koninck and Cooper, 1995), we measured gene expression of sympathetic neurons developing in culture. We found that these neurons express five nicotinic receptor transcripts: mRNA for α3 and β4 are the most abundant and increase over the first week in culture; mRNA for β2 and α5 are severalfold lower and remain constant, whereas mRNA for α7 is initially high but falls rapidly within 1-2 d in culture and remains low. Although there are no ...
Fingerprint Dive into the research topics of Effects of ethanol on acetylcholine and GABA release: differences in the role of potassium.. Together they form a unique fingerprint. ...
Opioids have been widely applied in clinics as one of the most potent pain relievers for centuries, but their abuse has deleterious physiological effects including immunosuppression. However, the mechanisms are unclear. TLRs and acetylcholine are widely expressed in the immune and nervous systems, and play critical roles in immune responses. In this article, we show that morphine suppresses the innate immunity in microglia and bone marrow-derived macrophages through differential regulation of TLRs and acetylcholinesterase. Either morphine or inhibition of acetylcholine significantly promotes upregulation of microRNA-124 (miR-124) in microglia, bone marrow-derived macrophages, and the mouse brain, where miR-124 mediates morphine inhibition of the innate immunity by directly targeting a subunit of NF-κB p65 and TNFR-associated factor 6 (TRAF6). Furthermore, transcription factors AP-1 and CREB inhibited miR-124, whereas p65 bound directly to promoters of miR-124, thereby enhancing miR-124 ...
A 125I-bungarotoxin labelling study of the acetylcholine receptor on the nerve-muscle junctions in the course of aging in the rat is reported. Attention is drawn to the fact that aging leads to an appreciable slowing down of the receptor degradation time, whereas no change occurs in its location.
After binding acetylcholine, the AChR responds by an extensive change in conformation that affects all subunits and leads to opening of an ion-conducting channel across the plasma membrane.
Studies in human beings and rodents support a job for muscarinic ACh receptor (mAChR) and nicotinic AChR in learning and storage, and both regulate hippocampal synaptic plasticity using organic and often situations opposing mechanisms. on the reduction in presynaptic discharge probability, likely due to tonic activation of mAChRs with the sustained upsurge in extracellular ACh. Hence these findings prolong current books by displaying that pharmacological AChE inhibition causes an extended reduction in presynaptic glutamate discharge at CA3-CA1 synapses, furthermore to inducing a most likely postsynaptic type of LTD. 0.05 was considered statistically significant. Data from electrophysiology tests had been filtered at 3 kHz, digitized at 10 kHz, and obtained using LabVIEW data acquisition software program. The slope from the increasing stage of fEPSP was assessed and plotted vs. period. Each stage represents the common of five fresh data points. To look for the magnitude of LTD, the slopes from ...
The fetal type acetylcholine receptor, composed of the alphabeta gammadelta subunits, has shown a highly variable channel kinetics during postnatal development. We examine the hypothesis whether such a variability could result from multiple channel forms, differing in the N-terminus of the gamma-sub …
We know that fish oil is a great source of Omega 3 fatty acids which can protect your brain, but did you know that pairing fish oil with Uridine can also increase the amount of acetylcholine in your brain by 30%?. We could all use more acetylcholine because it is a neurotransmitter which signals within the brain in areas, like the hippocampus, which control learning and memory. The body can synthesize acetylcholine from dietary choline, but it also uses a cycle called the Kennedy Cycle which utilizes Uridine (a nucleotide necessary for the Kennedy cycle) to make more phosphatidylcholine.. When DHA from fish oil is taken with Uridine, the levels of phosphatidylcholine in the brain increase by 30%! Increasing the amount of phosphatidylcholine means that your neurons can synthesize more acetylcholine which can boost your cognition and increase your ability to learn and remember.. Phosphatidylcholine is the final step in the Kennedy Cycle which neurons in the cholinergic pathway can use from which ...
When acetylcholine (neurotransmitter) binds to a receptor on the muscle fiber membrane, this stimulates ion channels to open which causes a certain influx
acetylcholine: A white crystalline derivative of choline, C7H17NO3, that is released at the ends of nerve fibers in the somatic and parasympathetic nervous systems and is involved in the transmission of nerve impulses in the body.
Speed your brain processing and decrease your stress! Acetylcholine is a neurotransmitter that plays a key role in keeping healthy the myelin sheath--fatty substance--that surrounds our neurons. When this sheath is healthy it conducts neural impulses faster, making our brain function…. ...
Acetylcholine is a chemical which is found in human nerves which are used to carry information regarding sense of touch, sense of smell, etc. This chemical is produced inside our brain in the pituitary gland. ...
Acetyl-CH Active (K-40) 90 Caps Acetyl-CH™ Active supports the cholinergic system and acetylcholine synthesis through the use of cofactors and precursors. Key ingredients include alpha-GPC,.... ...
Thornes Carnityl® (acetyl-L-carnitine) supports the health of the nerves in the upper and lower limbs and enhances the production of the neurotransmitter acetylcholine, which supports brain function.* Acetyl-L-carnitine also helps minimize the discomfort due to alterations in nerve function; for example, in cancer pat
Changes in the electric reactions of intact endothelium of isolated rat aorta were studied in conditions of aging. A value of resting membrane potential of endothelium of old rats (24-26 mo) was significantly greater, than in control group of animals (6 mo). In responses to acetylcholine and ATP the old rats did not show a typical course of reactions, which was peculiar to control animals. Inability of old rats to produce a typical response to acetylcholine and ATP may signify a disturbance of links between endothelial cells, which resulted in functional clusterization of the latter. The data obtained suggest a possible mechanism of decrease in production and release of potent vasodilator - nitric oxide - due to changes that occur in the electric properties of endothelium in aging ...
Neurotransmitters are chemical substances that transmit information from one nerve cell to another. Many types of neurotransmitters exist, each kind transmitting a specific type of information that participates in how the body functions. Acetylcholine: associated with muscle function; also associated with memory: Alzheimers Disease is marked by a 90% drop in acetylcholine Dopamine: associated with attention & learning, & motivation by gratification/reinforcement;…
Every time we spend time in the community, we find that there is a real need for proper nutrition. Despite all of our resources, there are still many people who simply do not get the resources that they need in order to perform their best. Many of the foods that we used to eat in our past are no longer consumed even though we have more abundance than we have ever had.. Its important to eat the right kinds of foods if you are trying to live a healthy lifestyle, but its also challenging when the options include kidney, liver, and other organ meats! In this article, we are going to talk about a few foods that everyone needs in their diet and a few of the ways that you can get there.. #1. Choline - one of the most important aspects of cognitive abilities is a molecule called choline. The choline molecule is the precursor for a compound called acetylcholine, which is something that has significant impacts on health. The acetylcholine neurotransmitter can help to increase brain capacity, memory ...
Thank you for your interest in spreading the word about Biochemical Society Transactions.. NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail. We do not capture any email address.. ...
Acetylcholine acts on the whole nervous system, from learning and memory to digestion, movement, and even sex. Learn the science here.
Hello, I will begin with what I have to offer, then will list what pokemon Im looking for. First and foremost, if you are wondering if youre eyes deceive you, let me assure you they do not. I have pokemon with the Pokerus virus! If you havent heard of this virus, I recommend getting very acquainted with it, as it is enormously rare to find and very helpful in building EVs for your pokemon. If you are also unfamiliar with EVs (effort values), a good deal of research is in order, as the
Shyng, S., Xu, R. and Salpeter, M. (1991). Cyclic AMP stabilizes the degradation of original junctional acetylcholine receptors in denervated muscle. Neuron, 6(3), pp.469-475 ...
Acetylcholine receptor antibody is a protein found in the blood of many people with myasthenia gravis. The antibody affects ... Acetylcholine receptor antibody is a protein found in the blood of many people with myasthenia gravis. The antibody affects ... 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 is used by bacteria, fungi, and a variety of other animals. Many of the uses of acetylcholine rely on its action ... Acetylcholine is the primary neurotransmitter of the parasympathetic nervous system. In the brain, acetylcholine functions as a ... In 1926, Loewi and E. Navratil deduced that the compound is probably acetylcholine, as vagusstoff and synthetic acetylcholine ... Nicotine binds to and activates nicotinic acetylcholine receptors, mimicking the effect of acetylcholine at these receptors. ...
Nicotinic acetylcholine receptor partial agonists. Class Summary. Nicotinic acetylcholine receptor partial agonists bind to ... Varenicline is a partial agonist selective for alpha4, beta2 nicotinic acetylcholine receptors. Its action is thought to result ...
Blocks action of acetylcholine at parasympathetic sites in smooth muscle, secretory glands, and CNS, which, in turn, has ... Blocks action of acetylcholine at parasympathetic sites in secretory glands, smooth muscle, and CNS. ... Binds to receptor sites on motor nerve terminals and inhibits release of acetylcholine, which, in turn, inhibits transmission ...
... the key physiological effects that result from stimulation of muscarinic receptors by excessive amounts of acetylcholine. ... Instead, when acetylcholine attaches to the external part of the muscarinic receptor, the internal portion of the receptor ... Muscarinic acetylcholine receptors - like nicotinic receptors - are proteins that extend through the cell membrane from the ... the key physiological effects that result from stimulation of muscarinic receptors by excessive amounts of acetylcholine. ...
... acetylcholine), frequency-based adverse effects, comprehensive interactions, contraindications, pregnancy & lactation schedules ... encoded search term (acetylcholine (Miochol E%2C)) and acetylcholine (Miochol E,) What to Read Next on Medscape ...
... the gene coding for the α7 nicotinic acetylcholine receptor (nAChR), and manifest a variable neuropsychiatric phenotype that ... The α7 nicotinic acetylcholine receptors regulate hippocampal adult-neurogenesis in a sexually dimorphic fashion *Simone L. ... Bidirectional Regulation of Aggression in Mice by Hippocampal Alpha-7 Nicotinic Acetylcholine Receptors. *Alan S Lewis ORCID: ... Freedman R (2014). Alpha7-nicotinic acetylcholine receptor agonists for cognitive enhancement in schizophrenia. Annu Rev Med 65 ...
Muscarinic Acetylcholine M2 Receptors Regulate Lateral Habenula Neuron Activity and Control Cocaine Seeking Behavior Clara I.C ... The Property-Based Practical Applications and Solutions of Genetically Encoded Acetylcholine and Monoamine Sensors Jun Chen, ... Nicotinic Acetylcholine Receptors Expressed by Striatal Interneurons Inhibit Striatal Activity and Control Striatal-Dependent ... Disrupted Choline Clearance and Sustained Acetylcholine Release In Vivo by a Common Choline Transporter Coding Variant ...
Acetylcholine receptor antibody Acetylcholine receptor antibody is a protein found in the blood of many people with myasthenia ... More About This Health Condition acetylcholine gamma muscle receptor subunit acetylcholine receptor subunit gamma ... ... acetyltransferase facilitates the production of a molecule called acetylcholine. Acetylcholine is essential for normal muscle ... of a larger protein called a neuronal nicotinic acetylcholine receptor (nAChR). Each nAChR protein is made up ... when attached ...
... Life Sci. 2007 May 30;80(24-25):2347-51. doi: ...
Neuronal acetylcholine receptors: fate of surface and internal pools in cell culture. J Stollberg and DK Berg ... Neuronal acetylcholine receptors: fate of surface and internal pools in cell culture ... Neuronal acetylcholine receptors: fate of surface and internal pools in cell culture ... Neuronal acetylcholine receptors: fate of surface and internal pools in cell culture ...
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Nonstandard abbreviations used: nicotinic acetylcholine receptor (nAchR); acetylcholine (Ach); N′Nitrosonornicotine (NNN); 4( ... Ligands for nicotinic acetylcholine receptors in human lung cancer cells. Biochem. Pharmacol. 1998. 55:1377-1384. View this ... A novel angiogenic pathway mediated by non-neuronal nicotinic acetylcholine receptors. J. Clin. Invest. 2002. 110:527-536. doi: ... Human and rodent bronchial epithelial cells express functional nicotinic acetylcholine receptors. Mol. Pharmacol. 1998. 54:779- ...
... products for your research including Nicotinic Acetylcholine R alpha 10/CHRNA10 Small Molecules and Nicotinic Acetylcholine R ... View our 3 Nicotinic Acetylcholine R alpha 10/CHRNA10 ... "Nicotinic Acetylcholine R alpha 10/CHRNA10" has 3 results in ...
... we investigated the action of hexamethonium on the major brain human nicotinic acetylcholine receptor (nAChR) stably expressed ... Amantadine inhibits nicotinic acetylcholine receptor function in hippocampal neurons.. *H. Matsubayashi, K. Swanson, E. ... Human α4β2 Neuronal Nicotinic Acetylcholine Receptor in HEK 293 Cells: A Patch-Clamp Study. *B. Buisson, M. Gopalakrishnan, S. ... Chronic Exposure to Nicotine Upregulates the Human α4β2 Nicotinic Acetylcholine Receptor Function. *B. Buisson, D. Bertrand ...
Welsh JH Marine invertebrate preparations useful in the bioassay of acetylcholine and 5-hydroxytryptamine Nature 1954 173:955 ... "Marine invertebrate preparations useful in the bioassay of acetylcholine and 5-hydroxytryptamine". ... "Marine invertebrate preparations useful in the bioassay of acetylcholine and 5-hydroxytryptamine" Nature. 1954;173:955. ...
Carroll, F., Navarro, H., Abraham, P., & Zhong, D. (2002). Ligands for .alpha.-7 nicotinic acetylcholine receptors based on ...
Structure of the M3 muscarinic acetylcholine receptor bound to the antagonist tiotropium crystallized with disulfide-stabilized ... Muscarinic acetylcholine receptor M3,Endolysin,Muscarinic acetylcholine receptor M3. A. 460. Rattus norvegicus, Escherichia ... Structure of the M3 muscarinic acetylcholine receptor bound to the antagonist tiotropium crystallized with disulfide-stabilized ...
Università degli Studi di Roma "La Sapienza" - Piazzale Aldo Moro 5, 00185 Roma. ...
... Does this test have other names?. Acetylcholine Receptor (AChR) Binding Antibody, AChR ... Acetylcholine is a chemical that helps muscles contract. It acts as a messenger between nerves and muscles. People who have ... This protein interferes with how acetylcholine works. At first, this causes muscle weakness in the eye. You may have double ... MG is an autoimmune disease because your body makes the antibody that attacks the way acetylcholine normally works. ...
Expression levels of brain nicotinic acetylcholine receptor mRNA and protein in coal-burning type of fluorosis rats.. Author: ... detect the expressions of neuronal nicotinic acetylcholine receptor(nAChR) at mRNA and protein levels in rat brains and to ...
Subtype-selective antagonists for muscarinic acetylcholine receptors (mAChRs) have long been elusive, owing to the highly ... Structure-based discovery of selective positive allosteric modulators of antagonists for the M2 muscarinic acetylcholine ... Subtype-selective antagonists for muscarinic acetylcholine receptors (mAChRs) have long been elusive, owing to the highly ... while sparing the endogenous agonist acetylcholine. NMR spectral changes determined for methionine residues reflected changes ...
Stimulation of acetylcholine release from myenteric neurons of guinea pig small intestine by forskolin and cyclic AMP.. W M Yau ... Stimulation of acetylcholine release from myenteric neurons of guinea pig small intestine by forskolin and cyclic AMP.. W M Yau ... Stimulation of acetylcholine release from myenteric neurons of guinea pig small intestine by forskolin and cyclic AMP.. W M Yau ... Stimulation of acetylcholine release from myenteric neurons of guinea pig small intestine by forskolin and cyclic AMP. ...
Ganglionic (alpha3) acetylcholine receptor antibodies have been reported in the sera of some patients with autoimmune autonomic ...
Mascia MS Cannabinoids decrease acetylcholine release in the medial-prefrontal cortex and hippocampus, reversal by SR 141716A ... "Cannabinoids decrease acetylcholine release in the medial-prefrontal cortex and hippocampus, reversal by SR 141716A". ... Most interestingly, SR 141716A alone at higher doses increased acetylcholine release both in the medial-prefrontal cortex (3 mg ... on the acetylcholine output in the medial-prefrontal cortex and hippocampus was studied by microdialysis in freely moving rats ...
Therefore, in this study, effects of BPA, vinclozolin and DDT-only and in combination with uterotonins (PGF-2α, acetylcholine ... p,0.05 as compared to ACh.† p,0.05 as compared to DDT n=6 animals per group ACH: acetylcholine. ... We further hypothesized that these compounds effect involved the uterotonin (PGF2α, acetylcholine and oxytocin) pathways. The ... p,0.05 compared to vinclozolin n=6 animals per group Ach: acetylcholine, Vin: vinclozolin. ...
Get up-to-date information on Acetylcholine side effects, uses, dosage, overdose, pregnancy, alcohol and more. Learn more about ... How was your experience with Acetylcholine?. First, a little about yourself. Male Female ...
Role of acetylcholine. Mirella Profita, Giusy Daniela Allbano, Caterina Di Sano, Angela Marina Montalbano, Rosalia Gagliardo, ... Role of acetylcholine. Mirella Profita, Giusy Daniela Allbano, Caterina Di Sano, Angela Marina Montalbano, Rosalia Gagliardo, ... Role of acetylcholine. Mirella Profita, Giusy Daniela Allbano, Caterina Di Sano, Angela Marina Montalbano, Rosalia Gagliardo, ... PBTh17 cells producing IL-17A and IL-22, as well as Acetylcholine (ACh) are involved in the systemic inflammation of several ...
acetylcholine binding / acetylcholine receptor activity / acetylcholine-activated cation-selective channel activity / ... Neuronal acetylcholine receptor subunit alpha-7. Details. Name. Neuronal acetylcholine receptor subunit alpha-7. Synonyms. * ... acetylcholine-gated channel complex / apical plasma membrane / asymmetric synapse / axolemma / cell junction / cytoplasm / ... After binding acetylcholine, the AChR responds by an extensive change in conformation that affects all subunits and leads to ...
Voltage-Independent Block of a Neuronal Nicottnic Acetylcholine Receptor by N-Methyl Lycaconitine DAVID B. SATTELLE, DAVID B. ... N-Methyl lycaconitine, neuronal nicotinic receptors, acetylcholine receptors, voltage-independent block, identified motor ... DAVID B. SATTELLE, ROBERT D. PINNOCK, SARAH C. LUMMIS; Voltage-Independent Block of a Neuronal Nicottnic Acetylcholine Receptor ... N-methyl lycaconitine completely blocked the response to ionophoretically applied acetylcholine recorded from the cell body ...
  • Drugs that act on muscarinic acetylcholine receptors, such as atropine, can be poisonous in large quantities, but in smaller doses they are commonly used to treat certain heart conditions and eye problems. (wikipedia.org)
  • The addictive qualities of nicotine are derived from its effects on nicotinic acetylcholine receptors in the brain. (wikipedia.org)
  • Like many other biologically active substances, acetylcholine exerts its effects by binding to and activating receptors located on the surface of cells. (wikipedia.org)
  • Nicotinic acetylcholine receptors are ligand-gated ion channels permeable to sodium, potassium, and calcium ions. (wikipedia.org)
  • Nicotinic acetylcholine receptor partial agonists bind to nicotine receptors and elicit mild nicotine central effects to ease withdrawal symptoms. (medscape.com)
  • Varenicline is a partial agonist selective for alpha4, beta2 nicotinic acetylcholine receptors. (medscape.com)
  • Identify the key physiological effects that result from stimulation of muscarinic receptors by excessive amounts of acetylcholine. (cdc.gov)
  • Muscarinic acetylcholine receptors - like nicotinic receptors - are proteins that extend through the cell membrane from the outside to the inside. (cdc.gov)
  • This smoking addiction results from nicotine acting on neuronal nicotinic acetylcholine receptors (nAchRs) in the brain in key regions controlling behavior. (jci.org)
  • To extend our knowledge of the pharmacological profile of human α4β2 neuronal nicotinic receptors, we investigated the action of hexamethonium on the major brain human nicotinic acetylcholine receptor (nAChR) stably expressed in human embryonic kidney 293 cells. (semanticscholar.org)
  • Subtype-selective antagonists for muscarinic acetylcholine receptors (mAChRs) have long been elusive, owing to the highly conserved orthosteric binding site. (nih.gov)
  • Peng X, Katz M, Gerzanich V, Anand R, Lindstrom J: Human alpha 7 acetylcholine receptor: cloning of the alpha 7 subunit from the SH-SY5Y cell line and determination of pharmacological properties of native receptors and functional alpha 7 homomers expressed in Xenopus oocytes. (drugbank.com)
  • UNLABELLED: Assays of human postmortem brain tissue have revealed that smokers have greater densities of high-affinity nicotinic acetylcholine receptors (nAChRs) in several brain regions than do nonsmokers or exsmokers. (duke.edu)
  • Regulation of E-cadherin-mediated adhesion by muscarinic acetylcholine receptors in small cell lung carcinoma. (rupress.org)
  • Anti-acetylcholine receptor antibody is found in 70-90% of patients with generalized acquired myasthenia gravis (MG). Lambert-Eaton syndrome is a close differential, as less than 13% of patients have clinical presentation similar to MG and antibodies against acetylcholine receptors in high titers. (medscape.com)
  • 2011) An auroradiographic survey of mouse brain nicotinic acetylcholine receptors defined by null mutants. (guidetopharmacology.org)
  • 2. Duvoisin RM, Deneris ES, Patrick J, Heinemann S. (1989) The functional diversity of the neuronal nicotinic acetylcholine receptors is increased by a novel subunit: beta 4. (guidetopharmacology.org)
  • Certain muscarinic acetylcholine receptors (mAChRs) have high affinity for organophosphate (OP) anticholinesterases, and their density is reduced by chronic exposure to OPs. (umaryland.edu)
  • Studies were conducted to optimize matrix-assisted laser desorption/ionization, time-of-flight mass spectrometry (MALDI TOF MS) in analyzing the composition of nicotinic acetylcholine receptors (nAChR) from Torpedo californica electric tissue in their membrane-bound, detergent-solubilized, and affinity-purified states. (elsevier.com)
  • Curare, for example, which has become known as the poison of the arrow, clearly demonstrates the importance of acetylcholine: it blocks the acetylcholine receptors and thus blocks the entire peripheral nervous system. (altmeyers.org)
  • Nicotine receptors (nicotinic acetylcholine receptors) are receptors that can be stimulated by nicotine. (altmeyers.org)
  • Nicotine contributes directly to lung carcinogenesis through the activation of nicotinic acetylcholine receptors (nAChRs). (umassmed.edu)
  • Neuronal nicotinic acetylcholine receptors (nAChRs) participate in diverse aspects of brain function and mediate behavioral and addictive properties of nicotine. (viewpoint.fr)
  • The receptor agonists and antagonists of acetylcholine may either directly affect the receptors or indirectly exert their effects, e.g. by affecting the acetylcholinesterase enzyme that degrades the ligand-receptor. (vedantu.com)
  • Myasthenia gravis syndrome, characterized by muscle weakness and fatigue, occurs when the body improperly develops antibodies to the nicotinic receptors of acetylcholine and thereby prevents the proper transmission of acetylcholine signals. (vedantu.com)
  • The recent identification of nicotinic acetylcholine receptors (nAChR) in pulmonary fibroblasts suggests that in utero nicotine exposure may alter collagen expression by these cells in the developing lung. (elsevier.com)
  • Crosstalk between beta-2-adrenoceptor and muscarinic acetylcholine receptors in the airway. (jefferson.edu)
  • Alcohol acts on multiple receptor systems including the nicotinic acetylcholine receptors (nAChRs), which are known to mediate alcohol consumption and reward. (umn.edu)
  • Nicotine is the primary psychoactive substance in tobacco, and it exerts its effects by interaction with various subtypes of nicotinic acetylcholine receptors (nAChRs) in the brain. (iawaketechnologies.com)
  • These compounds possess the anticholinergic properties as they could block the neurotransmitter acetylcholine action in the central and peripheral nervous system by binding at either muscarinic and/or nicotinic receptors. (springer.com)
  • Cholinergic receptors, addressed by both neuronal and non-neuronal (urothelial) acetylcholine, can alter neuronal excitability. (inrae.fr)
  • Thus we investigated the influence of BOO on the expression of muscarinic (mAChR) and nicotinic (nAChR) acetylcholine receptors in the lumbosacral dorsal root ganglia (DRG) of mice. (inrae.fr)
  • 20% of the acetylcholine receptors in cultured chick skeletal muscle remain unbound following long-term growth of muscle in medium containing a potent, essentially irreversible receptor-blocking agent, α-bungarotoxin. (elsevier.com)
  • The kinetics of labeling of the "pool" and "surface" receptors with 2 H, 13 C, 15 N-amino acids confirm the "precursor-product" type relationship of pool and surface acetylcholine receptors. (elsevier.com)
  • Activation of muscarinic acetylcholine receptors induces Ca(2+) mobilization in FRT cells. (unisalento.it)
  • 1. Studies were performed to determine whether antibodies prepared against nicotinic acetylcholine receptors (nAcChoR) from electric tissue are reactive toward nAcChoR-like antigenic determinants in rat brain. (barrowneuro.org)
  • The cell-surface topography and density of nicotinic acetylcholine receptors (nAChRs) play a key functional role in the synapse. (abberior.rocks)
  • The acetylcholine/vagus effects on pancreatic insulin release are mediated by activation of muscarinic acetylcholine receptors located on the pancreatic [beta]-cells (4-6). (indexarticles.com)
  • Interestingly, previous studies suggest that acetylcholine can also stimulate the secretion of glucagon by acting on muscarinic receptors located on pancreatic [alpha]-cells (5,6,26-28). (indexarticles.com)
  • The molecular basis of the inflammatory response to cerebral ischemia is poorly understood, but a role of nicotinic acetylcholine receptors (nAChRs) has been indicated 4 . (bruker.com)
  • The results indicate that nicotinic acetylcholine receptors could be energetic during adverse occasion setting which nicotine can potentiate discovered inhibition. (ly2090314.com)
  • Muscarinic acetylcholine receptors are known to play key roles in facilitating cognitive processes. (fujita-hu.ac.jp)
  • Activation of nicotinic acetylcholine receptors (nAChRs) in the IC can alter acoustic processing and enhance auditory task performance. (umich.edu)
  • Through a study of cloned nicotinic receptors expressed in Xenopus oocytes, we provide evidence that α-conotoxin IMI, a peptide marine snail toxin that induces seizures in rodents, selectively blocks subtypes of nicotinic acetylcholine receptors. (nau.edu)
  • α-Conotoxins thus represent selective tools for the study of neuronal nicotinic acetylcholine receptors. (nau.edu)
  • This compound is featured on the Acetylcholine Receptors (Muscarinic) page of the Handbook of Receptor Classification and Signal Transduction. (sigmaaldrich.com)
  • A simple assay for the study of solubilized acetylcholine receptors. (semanticscholar.org)
  • The studies Dr. Kistemaker described in her thesis have revealed that acetylcholine contributes to airway inflammation and remodeling in asthma and Chronic Obstructive Pulmonary Disease (COPD) specifically via M3 muscarinic receptors. (rug.nl)
  • When faced with abnormal muscle function, there are drugs that can block acetylcholine by binding to the cholinergic receptors. (naturalnews.com)
  • Many of the actions of these alkaloids are mediated by nicotinic acetylcholine receptors (nAChR). (usda.gov)
  • However, the data presented in this study suggest that the rat model is not a good model to study the teratogenicity of plant toxins that cause birth defects in livestock by inhibition of nicotinic acetylcholine receptors. (usda.gov)
  • The teratogenic action of some of these alkaloids is mediated by nicotinic acetylcholine receptors (nAChR). (usda.gov)
  • Humans with 15q13.3 microdeletion syndrome (15q13.3DS) are typically hemizygous for CHRNA7 , the gene coding for the α7 nicotinic acetylcholine receptor (nAChR), and manifest a variable neuropsychiatric phenotype that frequently includes persistent aggression. (nature.com)
  • The most common form of 15q13.3DS results from an ~1.5 megabase deletion that encompasses roughly six genes, including CHRNA7 , the gene encoding the excitatory ligand-gated α7 nicotinic acetylcholine receptor (nAChR). (nature.com)
  • of a larger protein called a neuronal nicotinic acetylcholine receptor (nAChR). (nih.gov)
  • To observe the learning and memory changes in coal-burning type of fluorosis rats, detect the expressions of neuronal nicotinic acetylcholine receptor(nAChR) at mRNA and protein levels in rat brains and to reveal the mechanism of changed learning and memory ability. (fluoridealert.org)
  • Our previous studies showed that α 7 nicotinic acetylcholine receptor (nAchR) agonist nicotine has stimulatory effects on murine bone marrow-derived semimature DCs, but the effect of nicotine on peripheral blood mononuclear cell- (PBMC-) derived human semimature dendritic cells (hu-imDCs) is still to be clarified. (hindawi.com)
  • In previous studies, we have demonstrated that ex vivo nicotine stimulation has stimulatory effects on murine bone marrow-derived semimature DCs (imDCs), which reveal efficient upregulation of surface molecules through α 7 nicotinic acetylcholine receptor (nAchR) [ 3 - 6 ]. (hindawi.com)
  • The nicotinic acetylcholine receptor (nAChR) is a ligandgated ion channel which is incorporated into the postsynaptic membrane of neurons [ 1 ]. (actanaturae.ru)
  • This protein shares 25% sequence homology with the extracellular domain of α7nAChrR (α7ED), and it is capable of interacting with some of the nAChR ligands (for example, acetylcholine, α-conotixins, and α-neurotoxins) [ 4 ]. (actanaturae.ru)
  • To identify the possible mutations and/or polymorphisms of neuronal nicotinic acetylcholine receptor (nAChR) genes related to the pathogenesis of sporadic AD, we have performed mutational analyses of the major neuronal nAChR genes (CHRNA3, 4, 7 and CHRNB2) expressed in central nervous system. (iospress.com)
  • Acetylcholine is a choline molecule that has been acetylated at the oxygen atom. (wikipedia.org)
  • Acetylcholine is synthesized in certain neurons by the enzyme choline acetyltransferase from the compounds choline and acetyl-CoA. (wikipedia.org)
  • The enzyme acetylcholinesterase converts acetylcholine into the inactive metabolites choline and acetate. (wikipedia.org)
  • Acetylcholine synthesis from radioactive choline was increased 100- to 1000-fold in the presence of non-neuronal cells from sympathetic ganglia. (caltech.edu)
  • Acetylcholine is formed by the enzyme choline acetyltransferase , an axoplasmic enzyme, from acetyl-CoA and choline. (altmeyers.org)
  • After binding to the acetylcholine receptor, ACh is rapidly cleaved by the enzyme acetylcholinesterase into choline and acetate, respectively, and thus inactivated. (altmeyers.org)
  • Owing to its multifaceted activity (non-selective) and rapid inactivation by choline, acetylcholine itself does not have therapeutic value as a drug for intravenous administration. (vedantu.com)
  • After release from the nerve ending, acetylcholine is rapidly inactivated by the enzyme acetylcholinesterase by hydrolysis to acetic acid and choline. (druglib.com)
  • The acetylcholine molecule is composed of an acetyl group and a choline moiety. (datatante.com)
  • When this group is attached to choline, it forms acetylcholine. (datatante.com)
  • [4] Choline is required to produce acetylcholine - a neurotransmitter - and S -adenosylmethionine (SAM), a universal methyl donor. (wikipedia.org)
  • You can take huge amounts of acetylcholine precursors such as choline or GPC without fear of acetylcholine overload because you have acetylcholinesterase to degrade excess acetylcholine. (digitalnaturopath.com)
  • The major precursor for acetylcholine in an essential nutrient called choline. (homida.com)
  • Choline has actually been examined for over a hundred years as well as supplementation could help battle some Acetylcholine deficiencies. (homida.com)
  • As a result, Choline ought to be eaten in the foods we eat or supplemented to prevent signs brought on by Acetylcholine deficiency. (homida.com)
  • Choline could enhance Acetylcholine production if levels are low in the mind. (homida.com)
  • Choline is in some cases called the "brain vitamin" because it is made use of to from Acetylcholine which contributes in state of mind guideline and has actually been examined for its results on stress and anxiety as well as depression. (homida.com)
  • Consequently, acetylcholine deficiency may become a condition that needs supplements along with a healthy diet regimen rich in choline. (homida.com)
  • To boost acetylcholine in the body, try to find foods abundant is necessary fats and B vitamins, particularly choline. (homida.com)
  • Acetylcholine is synthesized from acetyl coenzyme A and choline by the enzyme choline acetyltransferase. (sigmaaldrich.com)
  • In addition to its synthesis in the liver, choline employed in acetylcholine production is derived from dietary sources. (sigmaaldrich.com)
  • the gamma (γ) protein component (subunit) of the acetylcholine receptor (AChR) protein. (nih.gov)
  • making the epsilon (ε) component (subunit) of the acetylcholine receptor (AChR) protein. (nih.gov)
  • protein found in the muscle cell membrane called acetylcholine receptor (AChR). (nih.gov)
  • This test measures the concentration of a substance called acetylcholine receptor (AChR) antibody in your blood. (brighamandwomens.org)
  • After binding acetylcholine, the AChR responds by an extensive change in conformation that affects all subunits and leads to opening of an ion-conducting channel across the plasma membrane. (drugbank.com)
  • Neuregulin is a neural factor implicated in upregulation of acetylcholine receptor (AChR) synthesis at the neuromuscular junction. (elsevier.com)
  • Normally, no acetylcholine receptor (AChR) antibody exists in the bloodstream. (medscape.com)
  • We have investigated the role of the immunoglobulin-binding protein (BiP) in the folding and assembly of subunits of the acetylcholine receptor (AChR) in COS cells and in C2 muscle cells. (rupress.org)
  • On the postsynaptic muscular endplate ACh activates the acetylcholine receptor (AChR), a glycoprotein with an MG of 300kDa. (altmeyers.org)
  • Slow channel congenital myasthenic syndrome (SCCMS) is a disorder of the neuromuscular synapse caused by dominantly inherited missense mutations in genes that encode the muscle acetylcholine receptor (AChR) subunits. (ox.ac.uk)
  • Interactions between steroids and the nicotinic acetylcholine receptor (AChR) have been studied in native membrane vesicles from Torpedo marmorata electric organ by electron spin resonance (ESR) and fluorescence techniques. (okstate.edu)
  • The regulatory region of the neuronal nicotinic acetylcholine receptor α2 subunit gene, which contains six copies of the octamer-related sequence CCCCATGCAAT, is activated by the Brn-3b POU family transcription factor but not by the closely related factors Brn-3a and Brn-3c. (leedstrinity.ac.uk)
  • Furthermore, we show that acetylcholine excites VIP neurons directly and does not require intermediate activation of presynaptic inputs that might express nAChRs. (umich.edu)
  • Acetylcholine is the neurotransmitter used at the neuromuscular junction-in other words, it is the chemical that motor neurons of the nervous system release in order to activate muscles. (wikipedia.org)
  • Stimulation of acetylcholine release from myenteric neurons of guinea pig small intestine by forskolin and cyclic AMP. (aspetjournals.org)
  • The effect did not appear to be due to an increased plating efficiency of neurons, since the non-neuronal cells were capable of increasing acetylcholine synthesis after only 48-hr contact with neurons that had been previously grown without non-neuronal cells for 2 weeks. (caltech.edu)
  • None of the non-neuronal cell types synthesized detectable acetylcholine in the absence of the neurons. (caltech.edu)
  • Researchers have known that neurons that secrete acetylcholine are vulnerable in Alzheimer's disease, but so far, they have been unable to understand specifically how a lack of acetylcholine influences behavior. (brightfocus.org)
  • In addition, acetylcholine is found as a signalling substance in preganglionic sympathetic and in all parasympathetic neurons. (altmeyers.org)
  • Acetylcholine (ACh) is an organic chemical that acts as a neurotransmitter in the brain and body of several animal types (including humans), a chemical message produced by nerve cells to send signals to other cells, such as neurons, muscle cells, and cells of the gland. (vedantu.com)
  • Acetylcholine is processed at the ends of cholinergic neurons (producing acetylcholine) in vesicles. (vedantu.com)
  • Acetylcholine (ACh) is a neurotransmitter that is released from motor neurons and plays a critical role in muscle contraction. (datatante.com)
  • AIMS: In mammalian myocardium acetylcholine (ACh), neurotransmitter which strikingly affects the cardiomyocytes, can be released from the neurons both via quantal (vesicular) and nonquantal (non-vesicular) mechanism of secretion. (inrae.fr)
  • Using whole-cell electrophysiology in brain slices, we found that acetylcholine drives surprisingly strong and long-lasting excitation and inward currents in VIP neurons. (umich.edu)
  • Lastly, we found that low frequency trains of acetylcholine puffs elicited temporal summation in VIP neurons, suggesting that in vivo -like patterns of cholinergic input can reshape activity for prolonged periods. (umich.edu)
  • Certain neurotoxins work by inhibiting acetylcholinesterase, thus leading to excess acetylcholine at the neuromuscular junction, causing paralysis of the muscles needed for breathing and stopping the beating of the heart. (wikipedia.org)
  • The enzyme acetylcholinesterase acts so efficiently and quickly that only a few acetylcholine molecules leave the synaptic cleft by diffusion. (altmeyers.org)
  • While it is safe to boost acetylcholine levels by inhibiting acetylcholinesterase periodically, chronic use of Hup A could cause over-suppression of acetylcholinesterase and subsequent acetylcholine overload with unknown consequences. (digitalnaturopath.com)
  • Inhibition of acetylcholinesterase leads , thereby leading to an accumulation of acetylcholine in the central and peripheral nervous system. (cdc.gov)
  • Acetylcholinesterase, or AChE, breaks down the acetylcholine neurotransmitter. (dailyiowan.com)
  • Si, J, Wang, Q & Mei, L 1999, ' Essential roles of c-JUN and c-JUN N-terminal kinase (JNK) in neuregulin-increased expression of the acetylcholine receptor ε-subunit ', Journal of Neuroscience , vol. 19, no. 19, pp. 8498-8508. (elsevier.com)
  • Violin plots show distribution of expression levels for Neuronal acetylcholine receptor subunit alpha-7 (SMED30023488) in cells (dots) of each of the 12 neoblast clusters. (stowers.org)
  • Expression of Neuronal acetylcholine receptor subunit alpha-7 (SMED30023488) in the t-SNE clustered sub-lethally irradiated X1 and X2 cells. (stowers.org)
  • Violin plots show distribution of expression levels for Neuronal acetylcholine receptor subunit alpha-7 (SMED30023488) in cells (dots) of each of the 10 clusters of sub-leathally irradiated X1 and X2 cells. (stowers.org)
  • Nicotinic acetylcholine receptor alpha7 subunit is an essential regulator of inflammation. (bioseek.eu)
  • Here we report that the nicotinic acetylcholine receptor alpha7 subunit is required for acetylcholine inhibition of macrophage TNF release. (bioseek.eu)
  • Thus, the nicotinic acetylcholine receptor alpha7 subunit is essential for inhibiting cytokine synthesis by the cholinergic anti-inflammatory pathway. (bioseek.eu)
  • Allele-specific silencing of a pathogenic mutant acetylcholine receptor subunit by RNA interference. (ox.ac.uk)
  • Structure-based optimization led to compound '628, which enhanced binding of NMS, and the drug scopolamine itself, with a cooperativity factor (α) of 5.5 and a K B of 1.1 μM, while sparing the endogenous agonist acetylcholine. (nih.gov)
  • Recently, xanomeline, a muscarinic acetylcholine receptor (mAChR) agonist, has entered phase III clinical trials for the treatment of schizophrenia. (wustl.edu)
  • Varenicline, an alpha4beta2 nicotinic acetylcholine receptor partial agonist, vs sustained-release bupropion and placebo for smoking cessation: a randomized controlled trial. (medscape.com)
  • This explains why acetylcholine, unlike norepinephrine , does not appear in circulating blood. (altmeyers.org)
  • The influence of intrarenal acetylcholine (ACh) or intravenous furosemide (F) on the course of norepinephrine (NE)-induced acute renal failure (ARF) was investigated in the dog. (elsevier.com)
  • abstract = "Various concentrations of acetylcholine (ACh) were detected in samples of bovine, goat, horse, porcine, rat and sheep blood and plasma using a specific, sensitive radioimmunoassay. (elsevier.com)
  • Acetylcholine receptor antibody is a protein found in the blood of many people with myasthenia gravis . (medlineplus.gov)
  • This article discusses the blood test for acetylcholine receptor antibody. (medlineplus.gov)
  • Normally, there is no acetylcholine receptor antibody (or less than 0.05 nmol/L) in the bloodstream. (medlineplus.gov)
  • An abnormal result means acetylcholine receptor antibody has been found in your blood. (medlineplus.gov)
  • People who have myasthenia gravis (MG) often make an abnormal protein called acetylcholine receptor antibody. (brighamandwomens.org)
  • MG is an autoimmune disease because your body makes the antibody that attacks the way acetylcholine normally works. (brighamandwomens.org)
  • [ 1 ] Therefore the reflex panel detects anti-acetylcholine receptor (blocking and binding) antibodies in the serum, if antibody level is greater than 0.4nmol/L, or antibody level is greater than 15% then modulating antibody is added. (medscape.com)
  • More than 30% of patients with MG are seronegative (ie, anti-acetylcholine receptor antibody is absent in these patients). (medscape.com)
  • Neostigmine challenge and acetylcholine receptor antibody test were not consistent with myasthenia gravis. (cdc.gov)
  • Yi, Q & LEFVERT, ANNKARI 1993, ' Human Muscle Acetylcholine Receptor Reactive T and B Lymphocytes in Myasthenia Gravis ', Annals of the New York Academy of Sciences , vol. 681, no. 1, pp. 339-341. (houstonmethodist.org)
  • Muscle nicotinic acetylcholine receptor mRNA expression in hyperplastic and neoplastic myasthenia gravis thymus. (ox.ac.uk)
  • Ganglionic (alpha3) acetylcholine receptor antibodies have been reported in the sera of some patients with autoimmune autonomic neuropathy. (ouh.nhs.uk)
  • Antibodies against the M3 muscarinic acetylcholine receptor (M3R) are postulated to have inhibitory effects on parasympathetic neurotransmission in patients with Sjögren's syndrome (SS) leading to lacrimal and salivary glandular dysfunction. (cognizure.com)
  • Design of $\alpha$7 nicotinic acetylcholine receptor ligands in quinuclidine, tropane and quinazoline series. (archives-ouvertes.fr)
  • Acetylcholine (ACh) is an organic chemical that functions in the brain and body of many types of animals (including humans) as a neurotransmitter. (wikipedia.org)
  • In the brain, acetylcholine functions as a neurotransmitter and as a neuromodulator. (wikipedia.org)
  • Expression levels of brain nicotinic acetylcholine receptor mRNA and protein in coal-burning type of fluorosis rats. (fluoridealert.org)
  • Early cognitive symptoms of Alzheimer's disease can be improved by drugs that slow the breakdown of an important brain messenger called acetylcholine. (brightfocus.org)
  • Dr. Prado has hypothesized that these methodologies can now be used to selectively impair or decrease acetylcholine secretion in certain brain regions of the mouse. (brightfocus.org)
  • Certain behaviors can now be studied in these mice and their performance correlated with the levels of acetylcholine secretion in different brain regions. (brightfocus.org)
  • After γ-aminobutyric acid (GABA) and glycine , acetylcholine is one of the neurotransmitters most frequently found in the brain. (altmeyers.org)
  • Acetylcholine acts in the brain as a neurotransmitter and as a neuromodulator. (vedantu.com)
  • Acetylcholine (ACh) is an organic molecule that acts as a neurotransmitter in the brain. (datatante.com)
  • The isolation and characterization of acetylcholine-containing particles from brain. (wikidata.org)
  • Precursor to acetylcholine, a major neurotransmitter in the brain. (digitalnaturopath.com)
  • Acetylcholine is recognized for its function in enabling the brain to process and also accessibility information. (homida.com)
  • Largely located in the central nerves, the forerunners of acetylcholine go through numerous stages prior to becoming available to the brain. (homida.com)
  • Acetylcholine is a natural chemical that transfers nerve impulse throughout synapses in the brain and throughout the nerve system. (homida.com)
  • This enzyme also helps break down the brain chemical acetylcholine, which is linked to memory and learning. (livescience.com)
  • This nootropic compound is thought to increase acetylcholine levels in the brain. (dailyiowan.com)
  • Scientists do not yet fully understand how cholinesterase inhibitors work to treat Alzheimer's disease, but current research indicates that they prevent the breakdown of acetylcholine, a brain chemical believed to be important for memory and thinking. (psychcentral.com)
  • Binds to receptor sites on motor nerve terminals and inhibits release of acetylcholine, which, in turn, inhibits transmission of impulses in neuromuscular tissue. (medscape.com)
  • An enzyme that occurs especially in some nerve endings and in the blood and promotes the breakdown of acetylcholine. (cdc.gov)
  • In Alzheimer's disease there is a deficiency of acetylcholine due to the death of nerve cells that produce acetylcholine. (altmeyers.org)
  • however, the identity of the essential macrophage acetylcholine-mediated (cholinergic) receptor that responds to vagus nerve signals was previously unknown. (bioseek.eu)
  • In the peripheral nervous system, acetylcholine is released into the neuromuscular junction when a nerve impulse arrives at the terminal of a motor neuron. (vedantu.com)
  • Acetylcholine is a naturally occurring neurohormone which mediates nerve impulse transmission at all cholinergic sites involving somatic and autonomic nerves. (druglib.com)
  • A look at how multibanded krait snake venom interacts with the nicotinic acetylcholine receptor that mediates nerve activation of muscles. (ucsf.edu)
  • Acetylcholine, for instance, directly manages muscle contractions in the parasympathetic nerve system. (homida.com)
  • Acetylcholine is released from intrapancreatic parasympathetic (vagal) nerve endings during the preabsorptive and, most likely, the absorptive phase of feeding (5,6). (indexarticles.com)
  • Rings were subjected to exogenous contractile agonists (acetylcholine, histamine, endothelin-1, substance P, acetyl-substance P, and neurokinin A) or to electrical field stimulation (EFS) to differentiate cholinergic or nonadrenergic, noncholinergic nerve-mediated contraction with or without cumulatively increasing concentrations of propofol, thiopental, etomidate, or ketamine. (asahq.org)
  • 1 The presumed mechanism of airway protection by propofol involves the attenuation of parasympathetic nerve acetylcholine release: the assumed mechanism of irritant-induced bronchoconstriction. (asahq.org)
  • The vagus nerve releases a neurotransmitter called acetylcholine that catalyzes increased focus and calmness. (forbes.com)
  • A quohaug's heart is very sensitive to acetylcholine, material that is released at the end of the nerves, such as the vagus nerve, & that slows the heartbeat. (newyorker.com)
  • This research will provide fundamental knowledge on how a deficit of acetylcholine contributes to some of the symptoms associated with Alzheimer's disease. (brightfocus.org)
  • Acetylcholine levels are reduced during Alzheimer's. (livescience.com)
  • The inhibitory effect of delta9-tetrahydrocannabinol and WIN 55,212-2 was suppressed in both areas by the specific cannabinoid CB1 receptor antagonist, [N-(piperidin-1-yl)-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-me thyl-1H-pyrazole-3carboxamide]HCl (SR 141716A), at the dose of 0.1 mg/kg i.p., per se ineffective to modify basal acetylcholine release. (erowid.org)
  • Discovery and development of a potent and highly selective small molecule muscarinic acetylcholine receptor subtype I (mAChR 1 or M1) antagonist in vitro and in vivo probe. (vanderbilt.edu)
  • Preliminary synthetic studies of methyllycaconitine, a potent nicotinic acetylcholine receptor antagonist: rapid syntheses of AE-bicyclic analogues. (ox.ac.uk)
  • Miochol-E (acetylcholine chloride intraocular solution) is used to obtain miosis of the iris in seconds after delivery of the lens in cataract surgery, in penetrating keratoplasty, iridectomy and other anterior segment surgery where rapid miosis may be required. (nih.gov)
  • Miochol ® -E (acetylcholine chloride intraocular solution) is a parasympathomimetic preparation for intraocular use. (druglib.com)
  • Drugs that function on the acetylcholine system are either receptor agonists, activating the system, or inhibiting it with antagonists. (vedantu.com)
  • Blocks action of acetylcholine at parasympathetic sites in secretory glands, smooth muscle, and CNS. (medscape.com)
  • In medicine, there are many uses to inhibit, hinder, or imitate the action of acetylcholine. (vedantu.com)
  • Recently, a research group from the USA published the xray structure of acetylcholine binding protein (AchBP) from Lymnaea stagnalis [ 4 ]. (actanaturae.ru)
  • The administration of delta9-tetrahydrocannabinol (1 and 5 mg/kg i.p.) and WIN 55,212-2 (5 and 10 mg/kg i.p.) produced a long lasting inhibition of acetylcholine release in both areas. (erowid.org)
  • Visceral adipose tissue-derived serine protease inhibitor augments acetylcholine-induced relaxation via the inhibition of acetylcholine esterase activity in rat isolated mesenteric artery. (nii.ac.jp)
  • Acetylcholine is a substance produced by the body that functions as a neurotransmitter. (naturalnews.com)
  • blocking the effects of a certain natural substance ( acetylcholine ) on the central nervous system. (nih.gov)
  • Many cognitive processes are linked to acetylcholine as a messenger substance. (altmeyers.org)
  • acetyltransferase facilitates the production of a molecule called acetylcholine. (nih.gov)
  • The structure of the partial inclusion complex in which an acetylcholine molecule was encapsulated within the hemicryptophane was characterized by NMR, X-ray crystal structure, and ESI-MS analysis. (infona.pl)
  • Topical ocular instillation of acetylcholine to the intact eye causes no discernible response as cholinesterase destroys the molecule more rapidly than it can penetrate the cornea. (druglib.com)
  • In the PNS, acetylcholine activates muscles and is a major neurotransmitter in the autonomic nervous system. (wikipedia.org)
  • Acetylcholine is also a neurotransmitter in the autonomic nervous system, both as an internal transmitter for the sympathetic nervous system and as the final product released by the parasympathetic nervous system. (wikipedia.org)
  • Acetylcholine is the primary neurotransmitter of the parasympathetic nervous system. (wikipedia.org)
  • This enzyme is abundant in the synaptic cleft, and its role in rapidly clearing free acetylcholine from the synapse is essential for proper muscle function. (wikipedia.org)
  • The α7 nicotinic acetylcholine receptor is a pentameric ligand-gated ion channel that modulates neuronal excitability, largely by allowing Ca 2+ permeation. (bioexcel.eu)
  • A neurotransmitter called acetylcholine (or ACh) helps your muscles contract, as well as regulating functions as diverse as sweating, heart function, and pupil dilation. (scienceblogs.com)
  • Forskolin, an activator of adenylate cyclase, was used to examine the regulation of [3H]acetylcholine (ACh) release by cyclic AMP (cAMP)-related mechanisms in myenteric plexus-longitudinal muscle preparations of guinea pig small intestine. (aspetjournals.org)
  • Most interestingly, SR 141716A alone at higher doses increased acetylcholine release both in the medial-prefrontal cortex (3 mg/kg i.p.) and hippocampus (1 and 3 mg/kg i.p.), suggesting that acetylcholine output is tonically inhibited by endogenous cannabinoids. (erowid.org)
  • Since the inhibitory effect of delta9-tetrahydrocannabinol is produced by doses within those relevant to human use of marijuana, our results suggest that the negative effects of the latter on cognitive processes may be explained by its ability to reduce acetylcholine release in the medial-prefrontal cortex and hippocampus. (erowid.org)
  • The acetylcholine-mediated preabsorptive phase of insulin secretion, although relatively small compared with the total release of insulin after a meal, seems to be of particular importance for maintaining normal glucose tolerance (5,6). (indexarticles.com)
  • An important feature of the cholinergic regulation of pancreatic insulin release is that acetylcholine stimulates insulin release in a strictly glucose-dependent manner, becoming more and more effective as the plasma glucose concentration increases (5,6). (indexarticles.com)
  • Stimulate acetylcholine release. (nutrimedical.com)
  • The cardiac sympathetic co-transmitter galanin reduces acetylcholine release and vagal bradycardia: implications for neural control of cardiac excitability. (ox.ac.uk)
  • Moreover we hypothesize that galanin acts similarly to NPY by reducing vagal acetylcholine release via a receptor mediated, protein kinase-dependent pathway. (ox.ac.uk)
  • Galanin (500 nM) also significantly attenuated the release of (3)H-acetylcholine from isolated atria during field stimulation (5 Hz, n=5). (ox.ac.uk)
  • These results demonstrate that prolonged sympathetic activation releases the slowly diffusing adrenergic co-transmitter galanin in addition to NPY, and that this contributes to the attenuation in vagal bradycardia via a reduction in acetylcholine release. (ox.ac.uk)
  • This protein interferes with how acetylcholine works. (brighamandwomens.org)
  • Acetylcholine binding protein, 2xz5. (ucsf.edu)
  • Relative to acetylcholine (ACh), xanomeline was biased away from ERK1/2 phosphorylation and calcium mobilization compared to Gαi2 protein activation. (wustl.edu)
  • Microdialysis measurement of acetylcholine in rat hippocampus during severe insulin-induced hypoglycemia. (nel.edu)
  • Umegaki H, Yamaguchi Y, Suzuki Y, Iguchi A. Microdialysis measurement of acetylcholine in rat hippocampus during severe insulin-induced hypoglycemia. (nel.edu)
  • We show that activating the M3 muscarinic acetylcholine receptor (mAChR) rapidly induces E-cadherin-mediated adhesion in a small cell lung carcinoma (SCLC) cell line. (rupress.org)
  • Predicted to enable acetylcholine receptor binding activity and acetylcholine receptor inhibitor activity. (nih.gov)
  • Therefore, in this study, effects of BPA, vinclozolin and DDT-only and in combination with uterotonins (PGF-2α, acetylcholine and oxytocin) on the force and pattern of uterine contraction were observed. (medsci.org)
  • Acetylcholine (ACh) is an important neurotransmitter that is involved in many functions in the body, including muscle contraction, memory, heart rate and digestion. (datatante.com)
  • Contraction was induced by Acetylcholine. (ayushdhara.in)
  • Relaxations or spasmolytic effect was noticed on all the doses of Mishreya Arka against the contraction induced by Acetylcholine. (ayushdhara.in)
  • Background and aims The impact of vasomotion types on long-term clinical outcomes in patients with coronary artery spasm (CAS) induced by the acetylcholine provocation test (ACH-test) remains unclear. (elsevier.com)
  • Background: Long-term clinical outcome data according to severity of coronary artery spasm (CAS) as assessed by an intracoronary acetylcholine provocation test are limited in series of Asian patients. (elsevier.com)
  • 70% fixed stenosis) who underwent an acetylcholine provocation test were enrolled and divided into four groups according to CAS severity during the acetylcholine provocation test: negative, borderline positive, moderately positive and severely positive. (elsevier.com)
  • C6 rat glioma cells were also able to stimulate acetylcholine synthesis, but 3T3 mouse fibroblast cells had little or no effect. (caltech.edu)
  • Acetylcholine is essential to the production of movement through acting at neuromuscular junctions in the peripheral nervous system. (xeragenx.com)
  • How disrupting cholinergic synaptic transmission could produce chronic illness is unclear, but recent research indicates that acetylcholine also mediates communication between axons and oligodendrocytes. (cdc.gov)
  • An in vitro system for studying the ionophore properties of the nicotinic acetylcholine receptor from the electric organs of Torpedo californica was developed. (caltech.edu)
  • The muscarinic acetylcholine receptor M 2 , also known as the cholinergic receptor, muscarinic 2 , is a muscarinic acetylcholine receptor that in humans is encoded by the CHRM2 gene . (mdwiki.org)
  • Excess acetylcholine produces a predictable cholinergic syndrome consisting of copious respiratory and oral secretions, diarrhea and vomiting, sweating, altered mental status, autonomic instability, and generalized weakness that can progress to paralysis and respiratory arrest. (cdc.gov)
  • A response can be stimulated or blocked by acetylcholine and thus can have excitatory or inhibitory effects. (vedantu.com)