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 language||English (US)|
|Number of pages||6|
|State||Published - Nov 11 2008|
- stress-induced hypoalgesia
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