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• W2076680451 abstract "The involvement of the GABA-benzodiazepine receptor complex in the regulation of melanotropin secretion has been investigated using perfused frog neurointermediate lobes. The GABAA agonist 3-amino-1 propane sulfonic acid mimicked the biphasic effect of GABA on α-melanocyte-stimulating hormone secretion: a brief stimulation followed by an inhibition of melanotropin secretion. The GABAA antagonist SR 95531 (10−4 M) inhibited both stimulation and inhibition of α-melanocyte-stimulatmg hormone release induced by GABA (10−4 M). Since the inhibitory effect of baclofen (10−4 M) was partially antagonized by SR 95531 (10−4 M). it appears that the GABAergic control of α-melanocyte-stimulating hormone release is mainly achieved through activation of GABAA receptors. GABA-induced stimulation of α-melanocyte-stimulating hormone release was inhibited by tetrodotoxin (10−5 M), an Na--channel blocker, or nifedipine (10−5 M). a voltage-dependent Ca2+-channel blocker, suggesting that Na+ and Ca2+ ions are involved in the stimulatory phase of GABA action. Only central-type benzodiazepine binding site agonists such as clonazepam (10−4 M) modified α-melanocyte-stimulating hormone release. In fact, clonazepam (10−5 to 10−5 M) led to a dose-dependent potentiation of both GABA-induced stimulation and inhibition of α-melanocyte-stimulating hormone release. This potentiating effect was antagonized by the GABAA antagonist SR 95531 (10−4 M) or by the central-type benzodiazepine binding site antagonist flumazenil (10−4 M). whereas picrotoxin (10−4 M) abolished only the stimulatory phase. In contrast, the peripheral-type benzodiazepine binding site agonist Ro 5-4864 (10−4 M) was unable to potentiate the effects of GABA on α-melanocyte-stimulating hormone secretion. To investigate the possible involvement of endogenous benzodiazepine binding site ligands in the control of α-melanocyte-stimulating hormone secretion, a radioimmunoassay for the octadecaneuropeptide, a putative endogenous benzodiazepine binding site inhibitor, has been developed. High concentrations of octadecaneuropeptide-like material were found in neurointermediate lobe extracts, suggesting that this peptide may act as a regulator of the GABA-benzodiazepine receptor complex. The administration of synthetic octadecaneuropeptide (10−6 to 10−4 M) to perifused neurointermediate lobes markedly reduced the effects of GABA on α-melanocyte-stimulatmg hormone release. In addition, flumazenil (10−4 M) reversed the inhibitory action of octadecaneuropeptide on GABA-induced modulation of α-melanocyte-stimulating hormone release. Taken together, these results indicate that GABA acts on frog melanotrophs through a GABA receptor complex including a GABAA recognition site, a Cl- channel and a central-type benzodiazepine binding site. Activation of benzodiazepine receptors has the potential to modulate the effects of GABA on α-melanocyte-stimulating hormone secretion, the final response depending on the properties of the benzodiazepine-receptor ligand used: central-type benzodiazepine binding site agonists cause an enhancement of the response to GABA, whereas the endogenous peptidergic ligand octadecaneuropeptide attenuates the action of GABA." @default.
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• W2076680451 date "1989-01-01" @default.
• W2076680451 modified "2023-09-27" @default.
• W2076680451 title "Central-type benzodiazepines and the octadecaneuropeptide modulate the effects of GABA on the release of α-melanocyte-stimulating hormone from frog neurointermediate lobe in vitro" @default.
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• W2076680451 doi "https://doi.org/10.1016/0306-4522(89)90391-6" @default.
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