| ¿µ¹® | receptor | ÇÑ±Û | ¼ö¿ëü |
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| ¿µ¹® | acetylcholine | ÇÑ±Û | ¾Æ¼¼Æ¿Äݸ° |
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| nAChR | nicotinic acetylcholine receptor |
|---|---|
| AcChR | acetylcholine receptor |
| AChR | acetylcholine receptor |
| AChRAb | acetylcholine receptor antibody |
| AChRP | acetylcholine receptor protein |
| nAChR | Nicotinic acetylcholine receptor |
|---|---|
| nAcChoR | nicotinic acetylcholine receptor |
| nACh | Nicotinic acetylcholine |
| nAChR | Nicotinic ACh receptor |
| AChR | Acetylcholine Receptor |
| nicotinic acetylcholine receptor | Integral membrane protein of the postsynaptic membrane to which acetylcholine binds. The receptor contains an integral ion channel, as a result of binding of acetylcholine, ion channels in the subsynaptic membrane are opened. at the neuromuscular junction, the nicotinic acetylcholine receptor initiates muscle contraction. Currently the best characterised ion channel protein: made of a hetero pentamer of related subunits, although a homo pentamer is functional in insects. Structural studies show that the acetylcholine binding site and the ionic channel are part of the same macromolecular unit. The nAChR mediates rapid transduction events (1ms) whereas receptors activating G-protein coupled channels operate on slower time scales (millisecond to second range). (18 Nov 1997) |
|---|
| acetylcholine receptor antibodies | <neurology, investigation> A test used to measure the amount of antibodies to acetylcholine receptors on nerve endings. This is a diagnostic test for myasthenia gravis. A normal value is no antibodies in the bloodstream. Acetylcholine receptor (AChR) binding autoantibodies (i.e. Antibodies reactive with several epitopes other than the binding site for acetylcholine or alpha-bungarotoxin) are present in approximately 88% of patients with generalised myasthenia gravis, 70% of ocular myasthenia and in approximately 80% of myasthenia gravis in remission. Although serum concentrations of AChR binding autoantibodies do not in general correlate well with severity of weakness, there is typical decrease in concentration as weakness improves with immunosuppressive therapy. AChR blocking autoantibodies (i.e., antibodies reactive with the AChR binding site) are present in about 50% of patients with myasthenia gravis, 30% with ocular myasthenia gravis and 20% of myasthenia gravis in remission, AChR blocking autoantibodies are the only AChR autoantibodies present in about 1% of myasthenia gravis. AChR modulating autoantibodies (i.e., autoantibodies which cross-link AChRs and cause their removal from muscle membrane surfaces) are present in more than 90% of myasthenia gravis and occasionally are the only AchR autoantibodies detectable in mild, recent onset or ocular-restricted myasthenia gravis. Results for AChR modulating autoantibodies can be transiently false-positive due to curare-like drugs used during general anesthesia. AChR autoantibodies of one or more types are found in at least 80% of ocular myasthenia gravis. Although generally absent in neurological conditions other than myasthenia gravis(and consequently unlikely to cause confusion in neurodiagnosis), false-positive results for AChR autoantibodies occasionally occur in primary biliary cirrhosis, tardive dyskinesia, autoimmune thyroiditis, the elderly, amyotrophic lateral sclerosis patients treated with cobra venom and patients with thymoma in the absence of myasthenia gravis. Approximately 1% of patients with rheumatoid arthritis treated with D-penicillamine develop AChR autoantibodies and myasthenia gravis, both of which disappear when the drug is discontinued. Babies born to ~10% of myasthenia gravis mothers have a transient neonatal form of myasthenia gravis that responds well to anticholinesterase therapy and usually remits within 1 month as maternal IgG disappears. (29 Dec 1997) |
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| muscarinic acetylcholine receptor | Distinct from the nicotinic ACh receptor in having no intrinsic ion channel, the receptor is formed from one protein chain with 7 transmembrane regions. The receptors produce their effect via activation of GTP-binding proteins. (18 Nov 1997) |
| nicotinic cholinergic receptor | A class of receptors responsive to acetylcholine that also are activated by nicotine; ganglionic (including the adrenal medulla) and neuromuscular receptors. Two classes exist: nicotinic-neuronal and nicotinic-muscular. (05 Mar 2000) |
| acetylcholine | <chemical, neurology, physiology> A chemical found in vertebrate neurons that carries information across the synaptic cleft, the space between two nerve cells. (06 May 1997) |
| acetylcholine chloride | A miotic, administered as an ophthalmic solution for parasympathomimetic effect; used in cataract surgery. (05 Mar 2000) |
| receptors, nicotinic | One of the two major classes of cholinergic receptors. Nicotinic receptors were originally distinguished by their preference for nicotine over muscarine. They are generally divided into muscle-type and neuronal-type (previously ganglionic) based on pharmacology, molecular biology, and biophysical properties of the channels. (12 Dec 1998) |
| nicotinic | <chemistry> Pertaining to, or derived from, nicotine; nicotic; used specifically to designate an acid related to pyridine, obtained by the oxidation of nicotine, and called nicotinic acid. Source: Websters Dictionary (01 Mar 1998) |
| nicotinic acid | A precursor of NAD, that is a product of the oxidation of nicotine. (18 Nov 1997) |
| nicotinic acid amide | <biochemistry> Member of the water soluble B vitamin group, used in the production of fatty acids, steroids and cholesterol, deficiency is known as pellagra. Has cholesterol-lowering and vasodilating properties. (27 Sep 1997) |
| nicotinic acid maculopathy | Maculopathy observed in persons taking 3000 mg or more of nicotinic acid daily; normal vision returns after this medication is discontinued. (05 Mar 2000) |
| nicotinic acids | 2-, 3-, or 4-pyridinecarboxylic acids. Pyridine derivatives substituted with a carboxy group at the 2-, 3-, or 4-position. The 3-carboxy derivative (niacin) is active as a vitamin. (12 Dec 1998) |
| nicotinic agonists | Drugs that bind to and activate nicotinic cholinergic receptors (receptors, nicotinic). Nicotinic agonists act at postganglionic nicotinic receptors, at neuroeffector junctions in the peripheral nervous system, and at nicotinic receptors in the central nervous system. Agents that function as neuromuscular depolarising blocking agents are included here because they activate nicotinic receptors, although they are used clinically to block nicotinic transmission. (12 Dec 1998) |
| nicotinic alcohol | <chemical> 3-pyridinemethanol. A direct-acting peripheral vasodilator that causes flushing and may decrease blood pressure. It is used in vasospasm and threatened gangrene. Pharmacological action: vasodilator agents. Chemical name: 3-Pyridinemethanol (12 Dec 1998) |
| nicotinic antagonists | Drugs that bind to nicotinic cholinergic receptors (receptors, nicotinic) and block the actions of acetylcholine or cholinergic agonists. Nicotinic antagonists block synaptic transmission at autonomic ganglia, the skeletal neuromuscular junction, and at central nervous system nicotinic synapses. (12 Dec 1998) |
| nicotinic receptors | A class of cholinergic receptors on skeletal muscle cells that are linked to ion channels in the cell membrane. (05 Mar 2000) |
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