pubmed-article:2574062 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:2574062 | lifeskim:mentions | umls-concept:C0034650 | lld:lifeskim |
pubmed-article:2574062 | lifeskim:mentions | umls-concept:C0027882 | lld:lifeskim |
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pubmed-article:2574062 | lifeskim:mentions | umls-concept:C0205409 | lld:lifeskim |
pubmed-article:2574062 | lifeskim:mentions | umls-concept:C1704632 | lld:lifeskim |
pubmed-article:2574062 | lifeskim:mentions | umls-concept:C1280500 | lld:lifeskim |
pubmed-article:2574062 | lifeskim:mentions | umls-concept:C0871261 | lld:lifeskim |
pubmed-article:2574062 | lifeskim:mentions | umls-concept:C2911692 | lld:lifeskim |
pubmed-article:2574062 | lifeskim:mentions | umls-concept:C1706817 | lld:lifeskim |
pubmed-article:2574062 | lifeskim:mentions | umls-concept:C0445254 | lld:lifeskim |
pubmed-article:2574062 | lifeskim:mentions | umls-concept:C0205198 | lld:lifeskim |
pubmed-article:2574062 | pubmed:issue | 3 | lld:pubmed |
pubmed-article:2574062 | pubmed:dateCreated | 1990-1-25 | lld:pubmed |
pubmed-article:2574062 | pubmed:abstractText | 1. The effects of benzodiazepines and non-benzodiazepine compounds on the gamma-aminobutyric acid (GABA)-induced chloride current (ICl) were studied in frog isolated sensory neurones by use of a concentration-jump (termed 'concentration-clamp') technique, under single-electrode voltage-clamp conditions. The drugs used were classified into four categories as follows: full benzodiazepine receptor agonists (diazepam, clonazepam, nitrazepam, midazolam, clotiazepam and etizolam), partial agonists (CL 218,872, Ro 16-6028, Ro 17-1812 and Ro 23-0364), inverse agonists (Ro 15-3505, FG 7142 and beta-CCE) and a benzodiazepine receptor antagonist, Ro 15-1788 (flumazenil). 2. All full agonists at concentrations of 3 x 10(-6) M or less increased dose-dependently the peak amplitude of ICl elicited by 3 x 10(-6) M GABA to twice to three times larger than the control. However, no further augmentation of the GABA response was observed at concentrations of 1 x 10(-5) M or higher. Partial agonists also showed a dose-dependent augmentation of the GABA response at concentrations ranging from 3 x 10(-8) M to 3 x 10(-5) M, but their efficacies of augmentation of the GABA response were only about half or less of those of full agonists. Of the inverse agonists, beta-CCE had a unique dose-dependent effect on the GABA response. Beta-CCE reduced dose-dependently the GABA response at concentrations of less than 3 x 10(-6) M, but augmented it at concentrations of 3 x 10(-5) M and 6 x 10(-5) M. The inverse agonists reduced dose-dependently the GABA response. The benzodiazepine antagonist, flumazenil, slightly augmented the GABA response at concentrations between 3 x 10 7M and 3 x 10 5 M. 3. These results show clear differences in the effects on the GABA response between these four categories of compounds known to affect the benzodiazepine recognition site of the GABA/ benzodiazepine receptor-chloride channel complex. Our experimental system of frog isolated sensory neurones and a 'concentration-clamp' technique appears to be useful for evaluating efficacy of compounds on responses mediated by the GABA/benzodiazepine receptor-chloride channel complex. | lld:pubmed |
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pubmed-article:2574062 | pubmed:language | eng | lld:pubmed |
pubmed-article:2574062 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2574062 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:2574062 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:2574062 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:2574062 | pubmed:month | Nov | lld:pubmed |
pubmed-article:2574062 | pubmed:issn | 0007-1188 | lld:pubmed |
pubmed-article:2574062 | pubmed:author | pubmed-author:AkaikeNN | lld:pubmed |
pubmed-article:2574062 | pubmed:author | pubmed-author:FukudaTT | lld:pubmed |
pubmed-article:2574062 | pubmed:author | pubmed-author:YakushijiTT | lld:pubmed |
pubmed-article:2574062 | pubmed:author | pubmed-author:OyamaYY | lld:pubmed |
pubmed-article:2574062 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:2574062 | pubmed:volume | 98 | lld:pubmed |
pubmed-article:2574062 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:2574062 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:2574062 | pubmed:pagination | 735-40 | lld:pubmed |
pubmed-article:2574062 | pubmed:dateRevised | 2010-3-29 | lld:pubmed |
pubmed-article:2574062 | pubmed:meshHeading | pubmed-meshheading:2574062-... | lld:pubmed |
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pubmed-article:2574062 | pubmed:meshHeading | pubmed-meshheading:2574062-... | lld:pubmed |
pubmed-article:2574062 | pubmed:year | 1989 | lld:pubmed |
pubmed-article:2574062 | pubmed:articleTitle | Effects of benzodiazepines and non-benzodiazepine compounds on the GABA-induced response in frog isolated sensory neurones. | lld:pubmed |
pubmed-article:2574062 | pubmed:affiliation | Department of Physiology, Faculty of Medicine, Kyushu University, Fukuoka, Japan. | lld:pubmed |
pubmed-article:2574062 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:2574062 | pubmed:publicationType | In Vitro | lld:pubmed |
pubmed-article:2574062 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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