Linked Life Data

2575888

Source:http://linkedlifedata.com/resource/pubmed/id/2575888

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1990-3-6
pubmed:abstractText
Effects of benzodiazepines were investigated on the gamma-aminobutyric acid-induced modulation of the basal and veratridine-evoked catecholamine release from cultured bovine adrenal chromaffin cells. GABA by itself, caused catecholamine release and facilitated veratridine-evoked catecholamine release. Midazolam enhanced the GABA-evoked catecholamine release in a dose-related fashion and further facilitated the enhancement by GABA of the veratridine-evoked catecholamine release. Clonazepam, a selective central-type benzodiazepine receptor agonist, also enhanced the GABA-induced catecholamine release, whereas ethyl-beta-carboline-3-carboxylate, an inverse agonist of the benzodiazepine receptor, reduced the GABA-evoked catecholamine release. The dose-response curve of the GABA-evoked catecholamine release was shifted to the left by midazolam without affecting the maximal response to GABA. Facilitation by midazolam and clonazepam of the GABA action or inhibition by ethyl-beta-carboline-3-carboxylate was antagonized by RO15-1788, which by itself had no effect on the basal or GABA- and veratridine-evoked catecholamine release. These results suggest that the central-type benzodiazepine receptor participates in the GABAergic modulation of the catecholamine release from adrenal chromaffin cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0301-4533
pubmed:author
pubmed:issnType
Print
pubmed:volume
300
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
254-64
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:articleTitle
Benzodiazepines facilitate the stimulatory action of gamma-aminobutyric acid (GABA) on basal and veratridine-evoked catecholamine release from cultured bovine adrenal chromaffin cells.
pubmed:affiliation
Department of Pharmacology, Hiroshima University School of Dentistry, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't