Zolpidem is a widely used hypnotic agent acting at the GABAA receptor benzodiazepine site. On recombinant receptors, zolpidem displays a high affinity to α1‐GABAA receptors, an intermediate affinity to α2‐ and α3‐GABAA receptors and fails to bind to α5‐GABAA receptors. However, it is not known which receptor subtype is essential for mediating the sedative‐hypnotic action in vivo. Studying α1(H101R) mice, which possess zolpidem‐insensitive α1‐GABAA receptors, we show that the sedative action of zolpidem is exclusively mediated by α1‐GABAA receptors. Similarly, the activity of zolpidem against pentylenetetrazole‐induced tonic convulsions is also completely mediated by α1‐GABAA receptors. These results establish that the sedative‐hypnotic and anticonvulsant activities of zolpidem are due to its action on α1‐GABAA receptors and not on α2‐ or α3‐GABAA receptors. British Journal of Pharmacology (2000) 131, 1251–1254; doi:10.1038/sj.bjp.0703717
British Journal of Pharmacology – Wiley
Published: Dec 1, 2000
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