α2-Noradrenergic antagonist administration into the central nucleus of the amygdala blocks stress-induced hypoalgesia in awake behaving rats

J. P. Ortiz, L. N. Close, M. M. Heinricher, N. R. Selden

Research output: Contribution to journalArticle

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Abstract

Stress-induced hypoalgesia (SIH) is an adaptive behavioral phenomenon mediated in part by the amygdala. Acute stress increases amygdalar noradrenaline levels and focal application of α2-adrenoceptor agonists in the central nucleus of the amygdala (CeA) is antinociceptive. We hypothesized that α2-adrenoceptor antagonist administration into the CeA may block SIH. Bilateral microinjections of drug or saline via chronically implanted CeA cannulae were followed by either a period of restraint stress or rest. The nocifensive paw-withdrawal latency (PWL) to a focused beam of light was measured. PWLs were longer in restrained rats, constituting SIH. Microinjection of the α2-adrenoceptor antagonist idazoxan into the CeA prior to restraint blocked SIH. Idazoxan administration in unrestrained rats had no effect. Microinjection of the α2-adrenoceptor agonist clonidine in unrestrained rats caused dose dependent hypoalgesia, mimicking the effects of environmental stress. α2-Adrenoceptor function in the CeA is necessary for restraint-induced SIH.

Original languageEnglish (US)
Pages (from-to)223-228
Number of pages6
JournalNeuroscience
Volume157
Issue number1
DOIs
StatePublished - Nov 11 2008

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Keywords

  • clonidine
  • idazoxan
  • nociception
  • restraint
  • stress-induced hypoalgesia
  • α-adrenoceptor

ASJC Scopus subject areas

  • Neuroscience(all)

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