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Lack of mu-opioid receptor leads to an increase in the nmda receptor subunit mrna expression and nmda-induced convulsion

Academic Article
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Overview

authors

  • Jang, Choon-Gon
  • Lee, S. Y.
  • Loh, H. H.
  • Ho, I. K.

publication date

  • October 2001

journal

  • Molecular Brain Research  Journal

abstract

  • The present study investigated in situ hybridization of N-methyl-D-aspartate (NMDA) receptor (NR) subunit mRNA and convulsion induced by intracerebroventricular injection of NMDA, in order to examine changes in NMDA receptor function in mu-opioid receptor gene knockout mice. Levels of NR1 and NR2A subunit mRNA were significantly increased in the parietal cortex (8.4 and 10.6%, respectively) and hypothalamus (8.7 and 15.2%, respectively) in mu-opioid receptor knockout mice. Levels of NR2B subunit mRNA were noted to be increased in the parietal cortex (9.1%), thalamus (7.7%), and hypothalamus (10.4%) in mu-opioid receptor knockout mice. The ED(50) for NMDA-induced convulsion in wild-type mice was 0.20 microg/10 microl/mouse. The ED(50) in mu-opioid receptor knockout mice was 0.14 microg/10 microl/mouse. There is a significant difference in the potency ratio of wild-type mice versus knockout mice (potency ratio: 1.44, P < 0.05). These results indicate that mu-opioid receptor knockout mice are more sensitive to NMDA-induced convulsion. Therefore, these results suggest that absence of mu-opioid receptor gene is accompanied by changes in the NMDA receptor system which can modulate the synaptic excitability in the process such as convulsion or epilepsy.

subject areas

  • Animals
  • Epilepsy
  • Excitatory Amino Acid Agonists
  • Gene Expression
  • In Situ Hybridization
  • Injections, Intraventricular
  • Mice
  • Mice, Knockout
  • N-Methylaspartate
  • RNA, Messenger
  • Receptors, N-Methyl-D-Aspartate
  • Receptors, Opioid, mu
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Research

keywords

  • NMDA receptor
  • convulsion
  • knockout mouse
  • mRNA
  • mu-opioid receptor
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Identity

International Standard Serial Number (ISSN)

  • 0169-328X

Digital Object Identifier (DOI)

  • 10.1016/s0169-328x(01)00222-4

PubMed ID

  • 11597770
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Additional Document Info

start page

  • 105

end page

  • 111

volume

  • 94

issue

  • 1-2

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