Biological processes in benzodiazepine dependence
作者:
MALCOLM LADER,
期刊:
Addiction
(WILEY Available online 1994)
卷期:
Volume 89,
issue 11
页码: 1413-1418
ISSN:0965-2140
年代: 1994
DOI:10.1111/j.1360-0443.1994.tb03737.x
出版商: Blackwell Publishing Ltd
数据来源: WILEY
摘要:
AbstractThe indications for the benzodiazepines include anxiety, insomnia, muscle spasm and epilepsy and each disorder has a variety of biological substrates. Limbic structures and the neurotransmitters noradrenaline, 5‐HT and GABA have all been implicated. Benzodiazepines act on alloosteric receptor sites and potentiate the actions of GABA in modulating chloride ionophores across nerve membranes. These effects can be blocked by the benzodiazepine antagonist, flumazenil. The molecular pharmacology of the benzodiazepine‐GABA‐chloride receptor is complex, with a wide range of different subunits. Animal models of dependence have suggested that the changes associated with long‐term benzodiazepine use are related more to receptor‐effector coupling than to the receptor characteristics themselves. Thus, benzodiazepine agonists on long‐term use lose their efficacy, antagonists become partial inverse antagonists, and inverse agonists increase in efficacy. Various clinical implications are explored, including the use of flumazenil to prevent and to treat benzodiazepine withdrawa
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