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O'Donovan MC, Buckland PR, McGuffin P. Levels of GABAa receptor subunit mRNA in rat brain following flurazepam treatment. J Psychopharmacol. 1992;6(3):364-9doi: 10.1177/026988119200600304.
O'Donovan, M. C., Buckland, P. R., & McGuffin, P. (1992). Levels of GABAa receptor subunit mRNA in rat brain following flurazepam treatment. Journal of psychopharmacology (Oxford, England), 6(3), 364-9. https://doi.org/10.1177/026988119200600304
O'Donovan, M C, et al. "Levels of GABAa receptor subunit mRNA in rat brain following flurazepam treatment." Journal of psychopharmacology (Oxford, England) vol. 6,3 (1992): 364-9. doi: https://doi.org/10.1177/026988119200600304
O'Donovan MC, Buckland PR, McGuffin P. Levels of GABAa receptor subunit mRNA in rat brain following flurazepam treatment. J Psychopharmacol. 1992 Jan;6(3):364-9. doi: 10.1177/026988119200600304. PMID: 22291381.
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J Psychopharmacol. 1992 Jan;6(3):364-9. doi: 10.1177/026988119200600304.

Levels of GABAa receptor subunit mRNA in rat brain following flurazepam treatment.

Journal of psychopharmacology (Oxford, England)

M C O'Donovan, P R Buckland, P McGuffin

Affiliations

  1. Department of Psychological Medicine, University of Wales College of Medicine, Heath Park, Cardiff CF4 4XN, UK.

PMID: 22291381 DOI: 10.1177/026988119200600304

Abstract

The regulation of the subunit composition of GABA(A) receptors may be a mechanism by which tolerance to the effects of benzodiazepines occurs. We have investigated this hypothesis by examining the levels of mRNA which codes for the GABA(A) β1, 2, 3 and γ2 subunits. Male Wistar rats were injected once daily with either flurazepam or vehicle, sacrificed after treatment regimes of up to 32 days and the brain RNA isolated. The levels of specific mRNAs encoding the receptor subunits were measured relative to a β-actin standard. No changes were found in the levels of these mRNAs at any time points. Our results lend no support to the hypothesis that alterations in the β or γ2 subunit composition of GABA(A) receptors is the mechanism responsible for the development of tolerance to, or dependence on, benzodiazepines.

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