Abstract

Rats exposed to the stress of repeated exposure to a noxious heat source (52.5°C, hot plate) exhibit stress-induced analgesia, but reduced antinociception (detected using the tail-flick test) to the administration of β-endorphin into the periaqueductal gray region of the brain. This is accompanied by an anti-analgesic response (reduction in the stress-induced increase of tail flick latency) to doses of β-endorphin (0.03 nmol) lower than those usually associated with antinociception. These alterations are prevented and antinociceptive potency is maintained when rats are treated with cholecystokinin (CCK) antagonists intrathecally. The potency of L-365,260 and L-364,718, selective CCK B and CCK A receptor antagonists, respectively, correlated with their apparent affinities for CCK B receptors, suggesting that the altered sensitivity to β-endorphin is mediated via CCK B receptors.

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