| pubmed-article:9990087 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9990087 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:9990087 | lifeskim:mentions | umls-concept:C0003467 | lld:lifeskim |
| pubmed-article:9990087 | lifeskim:mentions | umls-concept:C0017785 | lld:lifeskim |
| pubmed-article:9990087 | lifeskim:mentions | umls-concept:C0040616 | lld:lifeskim |
| pubmed-article:9990087 | lifeskim:mentions | umls-concept:C0597298 | lld:lifeskim |
| pubmed-article:9990087 | lifeskim:mentions | umls-concept:C1704632 | lld:lifeskim |
| pubmed-article:9990087 | lifeskim:mentions | umls-concept:C0871261 | lld:lifeskim |
| pubmed-article:9990087 | lifeskim:mentions | umls-concept:C0011155 | lld:lifeskim |
| pubmed-article:9990087 | lifeskim:mentions | umls-concept:C0205217 | lld:lifeskim |
| pubmed-article:9990087 | lifeskim:mentions | umls-concept:C2911692 | lld:lifeskim |
| pubmed-article:9990087 | lifeskim:mentions | umls-concept:C1706817 | lld:lifeskim |
| pubmed-article:9990087 | lifeskim:mentions | umls-concept:C0205349 | lld:lifeskim |
| pubmed-article:9990087 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:9990087 | pubmed:dateCreated | 1999-3-25 | lld:pubmed |
| pubmed-article:9990087 | pubmed:abstractText | The larger isoform of the enzyme glutamate decarboxylase, GAD67, synthesizes >90% of basal levels of gamma-aminobutyric acid (GABA) in the brain. In contrast, the smaller isoform, GAD65, has been implicated in the fine-tuning of inhibitory neurotransmission. Mice deficient in GAD65 exhibit increased anxiety-like responses in both the open field and elevated zero maze assays. Additionally, GAD65-deficient mice have a diminished response to the anxiolytics diazepam and pentobarbital, both of which interact with GABA-A receptors in a GABA-dependent fashion to facilitate GABAergic neurotransmission. Loss of GAD65-generated GABA does not appear to result in compensatory postsynaptic GABA-A receptor changes based on radioligand receptor binding studies, which revealed no change in the postsynaptic GABA-A receptor density. Furthermore, mutant and wild-type animals do not differ in their behavioral response to muscimol, which acts independently of the presence of GABA. We propose that stress-induced GABA release is impaired in GAD65-deficient mice, resulting in increased anxiety-like responses and a diminished response to the acute effects of drugs that facilitate the actions of released GABA. | lld:pubmed |
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| pubmed-article:9990087 | pubmed:language | eng | lld:pubmed |
| pubmed-article:9990087 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9990087 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:9990087 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9990087 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:9990087 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:9990087 | pubmed:author | pubmed-author:HodgeCC | lld:pubmed |
| pubmed-article:9990087 | pubmed:author | pubmed-author:BaekkeskovSS | lld:pubmed |
| pubmed-article:9990087 | pubmed:author | pubmed-author:KarpS SSS | lld:pubmed |
| pubmed-article:9990087 | pubmed:author | pubmed-author:TecottL HLH | lld:pubmed |
| pubmed-article:9990087 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9990087 | pubmed:day | 16 | lld:pubmed |
| pubmed-article:9990087 | pubmed:volume | 96 | lld:pubmed |
| pubmed-article:9990087 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9990087 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9990087 | pubmed:pagination | 1698-703 | lld:pubmed |
| pubmed-article:9990087 | pubmed:dateRevised | 2010-9-13 | lld:pubmed |
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