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Related Experiment Videos

Glutamate in opioid dependence

I K Ho1, Y Z Feng, S Tokuyama

  • 1Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson 39216-4505, USA.

Nihon Shinkei Seishin Yakurigaku Zasshi = Japanese Journal of Psychopharmacology
|August 1, 1997
PubMed
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Butorphanol dependence in rodents involves kappa-opioid receptors and glutamate systems in the locus coeruleus. Withdrawal symptoms are linked to increased glutamate release in this brain region.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Addiction Research

Background:

  • Opioid analgesics like butorphanol have abuse liability despite different receptor profiles than morphine.
  • Understanding the neurobiological mechanisms of opioid dependence is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the role of kappa-opioid receptors, glutamatergic systems, and the locus coeruleus in butorphanol-induced opioid dependence.
  • To elucidate the neuropharmacology underlying opioid withdrawal.

Main Methods:

  • Utilized a rodent model to study butorphanol-induced dependence.
  • Employed in vivo microdialysis to measure extracellular glutamate levels in the locus coeruleus during withdrawal.
  • Administered exogenous glutamate via intracerebroventricular injection to mimic withdrawal symptoms.

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Main Results:

  • Butorphanol dependence in rodents is mediated by kappa-opioid receptor activation.
  • Acutely precipitated withdrawal from butorphanol leads to increased extracellular glutamate in the locus coeruleus.
  • Glutamate acting on N-methyl-D-aspartate receptors mimics the butorphanol withdrawal syndrome.

Conclusions:

  • Glutamate plays a significant role in the general phenomenon of opioid dependence.
  • The locus coeruleus is identified as a key site for glutamatergic mediation of opioid dependence.
  • Kappa-opioid receptor involvement offers novel insights into the neuropharmacology of opioid dependence.