Selective antagonists of benzodiazepines View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1981-04

AUTHORS

W Hunkeler, H Möhler, L Pieri, P Polc, E P Bonetti, R Cumin, R Schaffner, W Haefely

ABSTRACT

Benzodiazepines produce most, if not all, of their numerous effects on the central nervous system (CNS) primarily by increasing the function of those chemical synapses that use gamma-amino butyric acid (GABA) as transmitter. This specific enhancing effect on GABAergic synaptic inhibition is initiated by the interaction of benzodiazepines with membrane proteins of certain central neurones, to which drugs of this chemical class bind with high affinity and specificity. The molecular processes triggered by the interaction of these drugs with central benzodiazepine receptors, and which result in facilitation of GABAergic transmission, are still incompletely understood. Theoretically, benzodiazepines could mimic the effect of hypothetical endogenous ligands for the benzodiazepine receptors, although there is no convincing evidence for their existence; in vitro studies indicate that benzodiazepines might compete with a modulatory peptide which is present in the supramolecular assembly formed by GABA receptor, chloride ionophore and benzodiazepine receptor and which reduces the affinity of the GABA receptor for its physiological ligand. The mechanisms of action of benzodiazepines at the molecular level are likely to be better understood following our recent discovery of benzodiazepine derivatives, whose unique pharmacological activity is to prevent or abolish in a highly selective manner at the receptor level all the characteristic centrally mediated effects of active benzodiazepines. Here, we describe the main properties of a representative of this novel class of specific benzodiazepine antagonists. More... »

PAGES

514-516

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/290514a0

DOI

http://dx.doi.org/10.1038/290514a0

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1009399243

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/6261143


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