Relationship between stress-induced analgesia and the POMC/β-endorphin system in the pituitary: Changes in β-endor-phin biosynthesis in acutely and chronically stressed rats

Abstract

Acute stress is known to release ACTH and β-endorphin(β-End) concomitant y from the anterior lobe(AL) of the pituitary. Behaviorally, acute stress produces analgesia which is naloxone reversible and blockable by hypophysectomy or dexametha-sone. Moreover, upon chronic stress, the animals become toler ant and are no longer rendered analgesic by further acute stress. The experiments were carried out to determine whether stress induced biochemical changes in the pro-opiomelanocortin (POMC) system in the AL and the intermediate-posterior lobe (IPL) of rats. In a series of pulse-chase experiments, acute stress led to an increase in POMC biosynthesis and shorter half-life in the AL. However, when the animals were chronically stressed, the AL no longer exhibited increased POMC synthesis. On the other hand, in the IPL, acute stress did not produce any biochemical changes, but chronic stress led to an increase in POMC synthesis and shorter half-life. In addition, chronic stress produced an increase in the metabolism of β-End to the N-acetyl form in the IPL. These results suggest that AL and IPL are affected by acute and/or chronic exposure to stress in opposite directions and that the POMC system in AL may play an important role in stress-induced analgesia.