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  • Title: Benzodiazepines and barbiturate potentiate the pre- and postsynaptic gamma-aminobutyric acid (GABA)A receptor-mediated response in the enteric nervous system of guinea pig small intestine.
    Author: Taniyama K, Hashimoto S, Hanada S, Tanaka C.
    Journal: J Pharmacol Exp Ther; 1988 Apr; 245(1):250-6. PubMed ID: 2834538.
    Abstract:
    To determine whether or not presynaptic gamma-aminobutyric acid (GABA) receptors regulate the release of GABA, we examined properties of the presynaptic GABA receptor and compared the findings within the case of the postsynaptic GABA receptor, using the longitudinal muscle with myenteric plexus (L-M) preparation of guinea pig small intestine. Muscimol, but not baclofen, reduced the Ca++-dependent release of [3H]GABA evoked by high K+ in the presence of tetrodotoxin from L-M preparation of the small intestine preloaded with [3H]GABA. Bicuculline, picrotoxin and furosemide antagonized the effect of muscimol. Diazepam, clonazepam and pentobarbital potentiated the muscimol-induced inhibition of high K+-evoked release of [3H]GABA. The potentiating effect of clonazepam was antagonized by Ro 15-1788. Muscimol induced a Ca++-dependent and tetrodotoxin-sensitive release of [3H]acetylcholine from L-M preparation preloaded with [3H]choline. The effect of muscimol was antagonized by bicuculline, picrotoxin and furosemide. Diazepam, clonazepam and pentobarbital potentiated the muscimol-evoked release of [3H]ACh. The potentiation of muscimol effect by clonazepam was inhibited by Ro 15-1788. These results indicate that both the GABA autoreceptor and postsynaptic receptor may possess the same property which is related to benzodiazepine and barbiturate binding sites in the enteric nervous system of the guinea pig small intestine. The benzodiazepine binding site seems to be of central type.
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