Contribution of Glutamate Receptors to Benzodiazepine Withdrawal Signs.

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  • Tsuda Makoto
    Section of Neuropharmacology, Division of Pharmacology, National Institute of Health Sciences
  • Shimizu Norifumi
    Department of Pharmacology, Wakayama Medical College
  • Suzuki Tsutomu
    Department of Toxicology, School of Pharmacy, Hoshi University

Bibliographic Information

Published
1999
Resource Type
journal article
DOI
  • 10.1254/jjp.81.1
  • 10.1016/s0021-5198(19)30801-7
Publisher
The Japanese Pharmacological Society

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Description

Recent research has demonstrated that the receptor for glutamate, a major excitatory neurotransmitter, may play an important role in the expression of benzodiazepine withdrawal signs. This proposal is based on various observations. For example, antagonists for N-methyl-D-aspartate (NMDA), non-NMDA and metabotropic glutamate (mGlu) receptors can suppress the behavioral signs of benzodiazepine withdrawal in mice and rats. Furthermore, the NMDA receptor in the cerebrocortical area of diazepam-withdrawn rats is upregulated. Finally, the stimulation of phosphoinositide hydrolysis mediated by mGluR is enhanced in cerebrocortical slices from lorazepam-withdrawn mice. These findings show that the upregulation of signal transduction mediated by glutamate receptors during diazepam withdrawal plays a role in the neuroadaptive response responsible for the expression of diazepam withdrawal signs. Furthermore, ligands for glutamate receptors may be suitable targets for treating benzodiazepine withdrawal signs.

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