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Journal Article

Differential benzodiazepine pharmacology of mammalian recombinant GABAA receptorss

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Ewert,  Markus
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

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Seeburg,  Peter H.
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

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Citation

Blankenfeld, G., Ymer, S., Pritchett, D. B., Sontheimer, H., Ewert, M., Seeburg, P. H., et al. (1990). Differential benzodiazepine pharmacology of mammalian recombinant GABAA receptorss. Neuroscience Letters, 115(2-3), 269-273. doi:10.1016/0304-3940(90)90467-N.


Cite as: http://hdl.handle.net/21.11116/0000-0000-7E6D-A
Abstract
We compared gamma-aminobutyric acid (GABA)-activated currents and their modulation by benzodiazepines in cultured human cells transfected with complementary desoxyribonucleic acid (cDNA) encoding different GABAA receptor subunits. Flunitrazepam, a benzodiazepine agonist which potentiates GABA responses in both neurons and astrocytes was only effective in receptors containing the gamma 2 subunit (alpha 1 beta 1 gamma 2 and alpha 5 beta 1 gamma 2). The beta-carboline methyl-4-ethyl-6,7-dimethoxy-beta-carboline-3-carboxylate (DMCM) decreased GABA-activated currents in receptors composed of alpha 1 beta 1 gamma 1 and alpha 1 beta 1 gamma 2 subunits but increased GABA-activated currents in receptors containing the alpha 5 subunit (alpha 5 beta 1 gamma 1 and alpha 5 beta 1 gamma 2). These results strongly suggest that flunitrazepam and DMCM do not act on isosteric sites and that differences in the responsiveness of GABAA receptors to these compounds are based on different subunit compositions of GABAA receptors.