A non-beta-endorphinergic adenohypophyseal mechanism is essential for an analgetic response to stress.
The present paper examines the role of pituitary pools of beta-endorphin in mediating the elevation in nociceptive threshold produced by stress. A 5 min foot-shock stress, characterized as activating both central and pituitary systems of beta-endorphin (beta-EP) and eliciting a naloxone-attenuated elevation in tail-flick latency in rats, was employed. Both total hypophysectomy and selective ablation of the anterior lobe almost completely abolished stress-induced analgesia (SIA), whereas removal of the neuro-intermediate lobe alone proved ineffective. However, manipulation of the hypothalamus-pituitary-adrenal feedback system by administration of either the corticosteroid, dexamethasone, or the corticosteroid synthesis inhibitor, metyrapone, in neither case affected SIA. None of these surgical or pharmacological manoeuvres affected basal nociceptive threshold (BNT). These data indicate that although the integrity of the adenohypophysis is essential for the manifestation of SIA, an adenohypophyseal mechanism, probably involving neither ACTH nor beta-EP, is essential for the development of the analgesia which accompanies stress.
D000324:Adrenocorticotropic Hormone / Q000097:blood; D000818:Animals; D004723:Endorphins / Q000378:metabolism*; D008297:Male; D009619:Nociceptors / Q000502:physiology; D010146:Pain / Q000378:metabolism*; D010903:Pituitary Gland, Anterior / Q000378:metabolism*; D051381:Rats; D012684:Sensory Thresholds; D013312:Stress, Physiological / Q000378:metabolism*
D004723:Endorphins; D000324:Adrenocorticotropic Hormone