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• W2039836698 abstract "1 The abilities of some benzodiazepine-receptor agonists, antagonists and inverse agonists to modulate the inhibitory potency of the γ-aminobutyric acid (GABA)A-receptor agonist, isoguvacine, on the CA1 population spike recorded from slices of rat hippocampus, were determined. 2 Concentration-response curves were constructed of the extent to which the benzodiazepine-receptor ligands shifted the isoguvacine concentration-response curve to the left or right. These were compared to their displacement curves of [3H]-Ro15-1788 binding to rat hippocampal membranes under near physiological assay conditions. 3 The above comparisons suggest that the effect on the potency of isoguvacine produced by the benzodiazepine-receptor agonists, diazepam and flunitrazepam, and the partial agonists, Ro16-6028 and Ro17-1812, closely parallels their degree of benzodiazepine-receptor occupancy. Thus, the partial agonists, Ro16-6028 and Ro17-1812, were unable to produce as large a maximum response as the full agonists, diazepam and flunitrazepam. 4 The maximum effects produced by diazepam, flunitrazepam, Ro16-6028, Ro17-1812, the antagonist, propyl-β-carboline-3-carboxylate, and the inverse agonist, methyl-6, 7-dimethyl-4-ethyl-β-carboline-3-carboxylate (DMCM), on the potency of isoguvacine in the hippocampal slice corresponded to the change in their affinities produced by the addition of GABA in the radioligand binding studies (GABA-shift). This suggests that the changes in affinity of benzodiazepine-receptor ligands produced by GABAA-receptor activation reflects their ability to modify GABAA-receptor function. 5 The benzodiazepine-receptor antagonists, Ro15-1788 and CGS 8216, had apparent agonist and inverse agonist effects, respectively, on the potency of isoguvacine. These effects occurred at concentrations above those required for saturation of the benzodiazepine-receptor, as labelled by [3H]-Ro15-1788, and were not in agreement with the absence of any effect of GABAA-receptor stimulation in the GABA-shift experiments. This indicates that these events are not mediated by an action at the classical benzodiazepine-receptor site. 6 It is concluded that hippocampal GABAA-receptor function can be allosterically modulated in a manner consistent with the agonist/inverse-agonist model of benzodiazepine-receptor activation, and that compounds exist with varying efficacies throughout this range." @default.
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• W2039836698 date "1987-07-01" @default.
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• W2039836698 title "The affinities, potencies and efficacies of some benzodiazepine-receptor agonists, antagonists and inverse-agonists at rat hippocampal GABAA-receptors" @default.
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• W2039836698 doi "https://doi.org/10.1111/j.1476-5381.1987.tb11253.x" @default.
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