Linked Life Data

1327823

Source:http://linkedlifedata.com/resource/pubmed/id/1327823

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1992-11-20
pubmed:abstractText
The aim of this study was to gain further insight into the function of cortical GABAB receptors. In chloral hydrate-anaesthetized rats, microiontophoretic administration of the GABAB receptor blocker CGP 35348 induced a moderate increase in firing of spontaneously active neurons in the rostral and caudal sensorimotor cortex. This increase in cell firing was accompanied by a reduction in the baclofen-induced inhibition of cell activity. In contrast to the GABAA receptor antagonist bicuculline methiodide, CGP 35348 did not induce any paroxysmal discharges. The excitatory responses of rostral cortical neurons elicited by iontophoretically applied acetylcholine and quisqualate were potentiated in most neurons after both microiontophoretic and intravenous administration of CGP 35348. The potentiation was observed in the absence of any change in the spontaneous firing rate. These effects were dose-dependent for both routes of administration. The potentiation of the quisqualate response was reversed by intravenously applied baclofen. In conclusion, these findings suggest that cortical GABAB receptors are involved in the control of cortical neuronal excitability.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0014-2999
pubmed:author
pubmed:issnType
Print
pubmed:day
21
pubmed:volume
218
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
137-43
pubmed:dateRevised
2003-11-14
pubmed:meshHeading
pubmed:year
1992
pubmed:articleTitle
Increased acetylcholine and quisqualate responsiveness after blockade of GABAB receptors.
pubmed:affiliation
Research and Development Department, Ciba-Geigy Ltd. Basle, Switzerland.
pubmed:publicationType
Journal Article