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| GABA, gaba | gamma-aminobutyric acid |
|---|---|
| GABA | Gamma-Amino-Butyric Acid |
| GABAT, GABA-T | gamma-aminobutyric acid transaminase |
| ER | efficiency ratio; epigastric region; ejection rate; electroresection; emergency room; endoplasmic re... |
| RAR | rapidly adapting receptor; rat insulin receptor; retinoic acid receptor; right arm reclining; right ... |
| GABA(A)-R | GABA(A) receptor |
|---|---|
| GABA-T | GABA aminotransferase |
| GABA-IR | GABA immunoreactive |
| GABA-T | GABA transaminase |
| GABA(A) | GABA type A |
| GABA receptor | <physiology> Ligand gated chloride ion channel forming receptor opened by gamma aminobutyric acid. Two distinct types: A and B. A receptor: One of a family of neurotransmitter receptors with fast intrinsic ion channels that includes the glycine receptor and the nicotinic acetylcholine receptor. Distinct from another major receptor family, the muscarininc acetylcholine receptor and rhodopsin, with no intrinsic ion channel. The A receptor is specifically blocked by bicuculline. It consists of two pairs of protein chains forming an A2B2 complex, the A chains bind benzodiazepine and the B chains bind GABA. The 4 subunits are thought to form a tight group with the chloride channel in the middle. There is considerable similarity between the amino acid sequences of the receptor subunits and those of the nicotinic acetylcholine receptor suggesting that both receptors are derived from some evolutionary ancestor. See: amino acid receptor superfamily. B receptor: Brain receptor (80 kD) for the inhibitory neurotransmitter gamma amino butyric acid. Differs from the A receptor both in agonist specificity (baclofen is a specific agonist) and its effects on cells. It modulates intracellular calcium levels through a Go mediated effect on N type calcium channels and also lowers intracellular cAMP levels by an effect on adenylyl cyclase, thereby reducing the secretion of catecholamines. (05 Jan 1998) |
|---|
| GABA | <biochemistry> An important amino acid which functions as the most prevalent inhibitory neurotransmitter in the central nervous system. Gamma aminobutyric acid works in partnership with a derivative of Vitamin B-6, pyridoxine, to cross from the axons to the dendrites through the synaptic cleft, in response to an electrical signal in the neuron and inhibits message transmission. This helps control the nerve cells from firing too fast, which would overload the system. The action of gamma aminobutyric acid decreases epileptic seizures and muscle spasms by inhibiting electrical signals in this manner. Studies have shown that the site of action in the brain of benzodiazepams, including Valium, is directly coupled to the brain receptor for gamma aminobutyric acid. Acronym: GABA (05 Jan 1998) |
|---|---|
| gaba agents | Substances used for their pharmacological actions on gabaergic systems. Gabaergic agents include agonists, antagonists, degradation or uptake inhibitors, depleters, precursors, and modulators of receptor function. (12 Dec 1998) |
| gaba agonists | Drugs that bind to and activate gaba receptors (receptors, gaba). (12 Dec 1998) |
| gaba antagonists | Drugs that bind to but do not activate gaba receptors, thereby blocking the actions of endogenous gaba or gaba agonists. (12 Dec 1998) |
| GABA dehydrogenase | <enzyme> From crude mitochondrial fraction of rat brain; reported first product is gamma-aminocrotonic acid; p-iodonitrotetrazolium violet can serve as acceptor of electrons Registry number: EC 1.- (26 Jun 1999) |
| gaba modulators | Substances that do not act as agonists or antagonists but do affect the gaba receptor-ionophore complex. Gaba-a receptors (receptors, gaba-a) appear to have at least three allosteric sites at which modulators act: a site at which benzodiazepines act by increasing the opening frequency of gaba-activated chloride channels; a site at which barbiturates act to prolong the duration of channel opening; and a site at which some steroids may act. General anaesthetics probably act at least partly by potentiating gabaergic responses, but they are not included here. (12 Dec 1998) |
| GABA pathway | The pathway that ultimately converts 4-aminobutyrate to succinate; succinate is then converted to alpha-ketoglutarate, via the tricarboxylic acid cycle, which is then acted upon by glutamate dehydrogenase; glutamate is then decarboxylated to reform 4-aminobutyrate; an important pathway for those cells which make this neuroactive molecule. Synonym: GABA pathway. (05 Mar 2000) |
| GABA permease | <chemical> From aspergillus nidulans; uga4 is from saccharomyces cerevisiae Synonym: gamma-amino-n-butyrate permease, 4-aminobutyric acid permease, uga4 protein, uga4 gene product (26 Jun 1999) |
| receptors, gaba | Cell-surface proteins that bind gaba with high affinity and trigger changes that influence the behaviour of cells. Gaba-a receptors control chloride channels formed by the receptor complex itself. They are blocked by bicuculline and usually have modulatory sites sensitive to benzodiazepines and barbiturates. Gaba-b receptors act through g-proteins on several effector systems, are insensitive to bicuculline, and have a high affinity for l-baclofen. (12 Dec 1998) |
| receptors, gaba-a | Cell surface proteins which bind gaba and control an integral membrane chloride channel. Gaba-a receptors are the most prevalent inhibitory neurotransmitter receptors in the brain. Several isoforms have been cloned, and they belong to a superfamily which includes nicotinic receptors, glycine receptors, and 5ht-3 receptors. Most gaba-a receptors have separate modulatory sites sensitive to benzodiazepines and to barbiturates. (12 Dec 1998) |
| receptors, gaba-b | Cell surface proteins which bind gaba and influence cells via interactions with g-proteins. Gaba-b receptors are pharmacologically characterised by their insensitivity to the blocker bicuculline and sensitivity to the agonist l-baclofen. They are found both presynaptically and postsynaptically, and act variously by inhibition of adenylate cyclase, activation of phospholipase a2, activation of potassium channels, and inactivation of voltage-activated calcium channels. (12 Dec 1998) |
| 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) |
| amino acid receptor | <biochemistry> Ligand gated ion channels with specific receptors for amino acid transmitters. An extended protein superfamily that also includes subunits of the nicotinic acetylcholine receptor. (18 Nov 1997) |
| AMPA receptor | <cell biology> Glutamate operated ion channel. See: excitatory amino acid receptor channels. (05 Feb 1998) |
| ANP receptor | <molecular biology> Family of 3 receptors for atrial natriuretic peptide. ANP A and ANP B have intracellular guanylate cyclase and protein kinase like domains. ANP C, shares the extracellular ligand binding and transmembrane domains, but lacks the functional intracellular domains and is not thought to be involved in signal transduction. (18 Nov 1997) |
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