Opiate withdrawal induces narp in the extended amygdala

Research output: Contribution to journalArticlepeer-review

Abstract

The negative affective states associated with drug withdrawal produce long-lasting behavioral effects thought to play a central role in the development and maintenance of dependence. However, little is known about the molecular mechanisms mediating the long-term effects of drug withdrawal. Neuronal activity-regulated pentraxin (Narp) is a secreted neuronal immediate early gene (IEG) product that regulates AMPA receptor clustering at synapses. As both IEGs and changes in AMPA receptor trafficking mediate enduring forms of neuronal plasticity, we have assessed whether Narp could be involved in the molecular adaptations accompanying drug withdrawal. To this end, we checked the effect of opiate withdrawal on Narp expression in the extended amygdala, a brain region closely linked to the aversive effects of drug withdrawal. We found a marked increase in the number of Narp-positive cells in this region following opiate withdrawal triggered by either low doses of opiate antagonists or by 'natural withdrawal', removal of the morphine pellets used to induce dependence. In contrast, Arc, another 'effector' IEG, was not induced by opiate withdrawal. As expected, pretreatment of animals with clonidine, which blocks opiate withdrawal, suppresses Narp induction in this paradigm. These results implicate Narp in mediating the long-term, aversive behavioral effects induced by opiate withdrawal.

Original languageEnglish (US)
Pages (from-to)1606-1613
Number of pages8
JournalNeuropsychopharmacology
Volume28
Issue number9
DOIs
StatePublished - Sep 2003

Keywords

  • AMPA receptor
  • Amygdala
  • BNST
  • Immediate early gene
  • Neuronal pentraxin
  • Opiate withdrawal
  • Synaptic plasticity

ASJC Scopus subject areas

  • Pharmacology
  • Psychiatry and Mental health

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