A NON-BETA-ENDORPHINERGIC ADENOHYPOPHYSEAL MECHANISM IS ESSENTIAL FOR AN ANALGETIC RESPONSE TO STRESS

  • 1 January 1980
    • journal article
    • research article
    • Vol. 8  (3) , 343-353
Abstract
The role of pituitary pools of .beta.-endorphin (.beta.-EP) in mediating the elevation in nociceptive threshold produced by stress was studied. A 5 min foot-shock stress, characterized as activating both central and pituitary systems of .beta.-EP and eliciting a naloxone-attenuated elevation in tail-flick latency in rats, was employed. Total hypophysectomy and selective ablation of the anterior lobe almost completely abolished stress-induced analgesia (SIA); removal of the neuro-intermediate lobe alone proved ineffective. Manipulation of the hypothalamus-pituitary-adrenal feedback system by administration of the corticosteroid, dexamethasone or the corticosteroid synthesis inhibitor, metyrapone, in neither case affected SIA. None of these surgical or pharmacological maneuvers affected basal nociceptive threshold. Although the integrity of the adenohypophysis is essential for the manifestation of SIA, an adenohypophyseal mechanism, probably involving neither ACTH nor .beta.-EP, apparently is essential for the development of the analgesia which accompanies stress.