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  • Title: Benzodiazepines and neurotransmitters.
    Author: Costa E.
    Journal: Arzneimittelforschung; 1980; 30(5a):858-61. PubMed ID: 6106485.
    Abstract:
    Benzodiazepines have been shown to change the turnover rate of 5-HT, ACh and catecholamines stored in selected brain areas, but the doses required for these effects are several-fold higher than those which elicit a persistent punished behavior or antagonize isoniazid, bicuculline or picrotoxin convulsion. The selective antagonism against convulsions elicited by drugs that impair GABAergic transmission, the capability of muscimol and other GABA receptors agonists to mimic behavioral and anticonvulsant action of the benzodiazepines have suggested that benzodiazepines facilitate GABA transmission. This facilitation of the GABA tranmission is due to an allosteric facilitation of high-affinity GABA binding to postsynaptic receptors. Also, the high-affinity binding of the benzodiazepines can be facilitated by GABA mimetics. Endogenous inhibitors of the benzodiazepines and GABA binding extracted from synaptic membranes play a role in facilitating these interactions. Using neuroblastoma 2A cells as a model and Cl- influx as an index of GABA receptor activation, it will be shown that the benzodiazepines facilitates not only GABA binding but also its action on Cl- channels. Also, glioma C6 cells have high affinity receptors for GABA and benzodiazepine binding but these binding sites are not linked to a Cl- channel. It is concluded that the benzodiazepines displace a regulatory protein for high-affinity GABA receptors and thereby facilitate GABAergic transmission.
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