| GABA, gamma-hydroxybutyric acid, and neurological disease. | |
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MedLine Citation:
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PMID: 12891648 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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gamma-Aminobutyric acid (GABA) is the primary inhibitory neurotransmitter in the central nervous system. GABA is converted from glutamic acid by the action of glutamic acid decarboxylase (GAD) of which two isoforms exist GAD65 and GAD67. GABA then is broken down, both within the cell and in the synaptic cleft by GABA transaminase to form succinic semialdehyde. In turn, succinic semialdehyde is converted either to succinic acid by succinic semialdehyde dehydrogenase or into gamma-hydroxybutyric acid (GHB) by succinic semialdehyde reductase. Because GABA modulates the majority of inhibition that is ongoing in the brain, perturbations in GABAergic inhibition have the potential to result in seizures. Therefore, the most common disorder in which GABA is targeted as a treatment is epilepsy. However, other disorders such as psychiatric disease, spasticity, and stiff-person syndrome all have been related to disorders of GABAergic function in the brain. This review covers the roles of GABAergic neurotransmission in epilepsy, anxiety disorders, schizophrenia, stiff-person syndrome, and premenstrual dysphoric disorder. In the final section of this review, the GABA metabolite GHB is discussed in terms of its physiological significance and its role in epilepsy, sleep disorders, drug and alcohol addiction, and an inborn error of GABA metabolism, succinic semialdehyde dehydrogenase deficiency. |
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Authors:
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C Guin Ting Wong; Teodoro Bottiglieri; O Carter Snead |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Review |
Journal Detail:
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Title: Annals of neurology Volume: 54 Suppl 6 ISSN: 0364-5134 ISO Abbreviation: Ann. Neurol. Publication Date: 2003 |
Date Detail:
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Created Date: 2003-07-31 Completed Date: 2003-12-24 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 7707449 Medline TA: Ann Neurol Country: United States |
Other Details:
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Languages: eng Pagination: S3-12 Citation Subset: IM |
Affiliation:
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Institute of Medical Sciences, University of Toronto, Faculty of Medicine and Brain and Behavior Research Program, Hospital for Sick Children, Ontario, Canada. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Aldehyde Oxidoreductases
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deficiency,
genetics Animals Humans Mice Nervous System Diseases / genetics*, metabolism Receptors, GABA-A / physiology Receptors, GABA-B / physiology Sodium Oxybate / metabolism*, pharmacology Succinate-Semialdehyde Dehydrogenase gamma-Aminobutyric Acid / physiology* |
| Chemical | |
Reg. No./Substance:
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0/Receptors, GABA-A; 0/Receptors, GABA-B; 502-85-2/Sodium Oxybate; 56-12-2/gamma-Aminobutyric Acid; EC 1.2.-/Aldehyde Oxidoreductases; EC 1.2.1.24/ALDH5A1 protein, human; EC 1.2.1.24/Succinate-Semialdehyde Dehydrogenase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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