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Gastrodia elata Bl attenuates cocaine-induced conditioned place preference and convulsion, but not behavioral sensitization in mice: importance of GABA(A) receptors

Academic Article
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Overview

authors

  • Shin, E. J.
  • Bach, J. H.
  • Nguyen, T. T. L.
  • Jung, B. D.
  • Oh, K. W.
  • Kim, M. J.
  • Jang, Choon-Gon
  • Ali, S. F.
  • Ko, S. K.
  • Yang, C. H.
  • Kim, H. C.

publication date

  • March 2011

journal

  • Current Neuropharmacology  Journal

abstract

  • It has been suggested that GABAergic neurotransmission can modulate cocaine dependence and seizure activity. Since Gastrodia elata Bl (GE), an oriental herb agent, has been shown to enhance GABAergic transmission, we examined whether GE affects cocaine-induced seizures, conditioned place preference (CPP), and behavioral sensitization in mice. Treatment with GE (500 or 1000 mg/kg, p.o.) significantly delayed seizure onset time and significantly shortened seizure duration induced by cocaine (90 mg/kg, i.p.). In addition, cocaine (15 mg/kg, i.p.)-induced CPP was significantly attenuated by GE in a dose-dependent manner. However, GE did not significantly alter behavioral sensitization induced by cocaine (15 mg/kg, i.p.). In order to understand whether GABAergic receptors are implicated in GE-mediated pharmacological action in response to cocaine, GABA(A) receptor antagonist bicuculline and GABA(B) receptor antagonist SCH 50911 were employed in the present study. GE-mediated attenuations on the cocaine-induced seizures and CPP were significantly reversed by bicuculline (0.25 or 0.5 mg/kg, i.p.), but not by SCH 50911 (1.5 or 3.0 mg/kg, i.p.). Therefore, our results suggest that GE attenuates cocaine-induced seizures and CPP via, at least in part, GABA(A) receptor activation.
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Research

keywords

  • GABA(A) receptors
  • Gastrodia elata Bl
  • cocaine
  • conditioned place preference
  • seizure
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Identity

PubMed Central ID

  • PMC3137195

International Standard Serial Number (ISSN)

  • 1570-159X

Digital Object Identifier (DOI)

  • 10.2174/157015911795017326

PubMed ID

  • 21886556
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Additional Document Info

start page

  • 26

end page

  • 29

volume

  • 9

issue

  • 1

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