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Actions of steroids and bemegride on the GABAA receptor of mouse spinal neurones in culture
Author(s) -
Mistry DK,
Cottrell GA
Publication year - 1990
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/expphysiol.1990.sp003394
Subject(s) - gabaa receptor , bicuculline , chemistry , gaba receptor antagonist , chloride channel , receptor , picrotoxin , antagonist , pharmacology , neuroscience , endocrinology , medicine , biology , biochemistry
The effects of a synthetic and an endogenous steroid were studied on the GABAA receptors of isolated mouse spinal neurones, maintained in culture. Low doses of alphaxalone reversibly increased GABA‐evoked whole‐cell currents. Alphaxalone at higher doses (10‐50 microM), when pressure ejected onto spinal neurones, also directly evoked a membrane chloride current. Such currents were reversibly suppressed by bicuculline (a GABAA antagonist) and enhanced by phenobarbitone. 5 beta‐Pregnan‐3 alpha‐ol‐20‐one, a progesterone metabolite, dose‐dependently potentiated the amplitude of GABA‐evoked whole‐cell currents. The mechanism of potentiation was examined at the single‐channel level using outside‐out patches from spinal neurones. The main action of the steroid on the GABAA receptor appears to be similar to that found for barbiturates, in that they prolonged GABA‐activated bursts of channel openings. Bemegride had an antagonistic action on the GABAA receptor, suppressing both GABA‐ and pentobarbitone‐evoked whole‐cell currents to similar extents.