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Curr Pharm Des ; 5(5): 317-43, 1999 May.
Artículo en Inglés | MEDLINE | ID: mdl-10213798

RESUMEN

Gamma-Aminobutyric acid (GABA) is the major inhibitory neurotransmitter in the mammalian Central Nervous System (CNS). GABA participates in the regulation of neuronal excitability through interaction with specific membrane proteins (the GABAA receptors). The binding of GABA to these postsynaptic receptors, results in an opening of a chloride channel integrated in the receptor which allows the entry of Cl- and consequently leads to hyperpolarization of the recipient cell. The action of GABA is allosterically modulated by a wide variety of chemical entities which interact with distinct binding sites at the GABAA receptor complex. One of the most thoroughly investigated modulatory site is the benzodiazepine binding site. The benzodiazepines constitute a well-known class of therapeutics displaying hypnotic, anxiolytic and anticonvulsant effects. Their usefulness, however, is limited by a broad range of side effects comprising sedation, ataxia, amnesia, alcohol and barbiturate potentiation, tolerance development and abuse potential. Consequently, there has been an intensive search for modulatory agents with an improved profile, and a diversity of chemical entities distinct from the benzodiazepines, but with GABA modulatory effects have been identified. The existence of endogenous ligands for the GABAA receptor complex beside GABA has often been described, but their role in the regulation of GABA action is still a matter of controversy. The progress of molecular biology during the last decade has contributed enormously to the understanding of benzodiazepine receptor pharmacology. A total of 14 GABAA receptor subunits have been cloned from mammalian brain and have been expressed/co-expressed in stable cell lines. These transfected cells constitute an important tool in the characterization of subtype selective ligands. In spite of the rapidly expanding knowledge of the molecular and pharmacological mechanisms involved in GABA/benzodiazepine related CNS disorders, the identification of clinically selective acting drugs is still to come.


Asunto(s)
Ansiolíticos/metabolismo , Ansiolíticos/farmacología , Agonistas del GABA/metabolismo , Agonistas del GABA/farmacología , Antagonistas del GABA/metabolismo , Antagonistas del GABA/farmacología , Receptores de GABA-A/efectos de los fármacos , Receptores de GABA-A/metabolismo , Animales , Benzodiazepinas , Sitios de Unión , Encéfalo/efectos de los fármacos , Encéfalo/metabolismo , Encéfalo/ultraestructura , Diseño de Fármacos , Agonistas de Receptores de GABA-A , Antagonistas de Receptores de GABA-A , Humanos , Ligandos
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