A PERMISSIVE ROLE OF CORTICOSTERONE IN AN OPIOID FORM OF STRESS-INDUCED ANALGESIA - BLOCKADE OF OPIATE ANALGESIA IS NOT DUE TO STRESS-INDUCED HORMONE-RELEASE

The 100 inescapable tail-shock paradigm produces three sequential anal gesic states as the number of shocks increases: an early opioid analge sia (after 2 shocks) that is attenuated by systemic naltrexone, a midd le analgesia (after 5-40 shocks) that is unaffected by systemic naltre xone, and a late opioid analgesia (after 80-100 shocks) that is attenu ated by systemic naltrexone. In order to determine whether the absence of adrenal hormones would affect any of these analgesias, we tested a drenalectomized (ADX) versus sham-operated control rats 2 weeks post-s urgery. Pain threshold was assessed using the tail-nick (TF) test. ADX attenuated both the early (2 shock) and late (80-100 shock) opiate an algesias and failed to reduce the naltrexone-insensitive analgesia aft er 5-40 shocks. We demonstrated that a loss of adrenomedullary catecho lamines does not underlie the ADX-induced attenuation of opioid analge sia since sympathetic blockade using systemic chlorisondamine (6 mg/kg ) failed to reduce analgesia at any point in the shock session. It was further shown that stress levels of adrenal hormones are not critical since (a) analgesia was unaffected when animals were tested 48 h afte r ADX, (b) 2 shocks do not produce a surge in corticosterone (CORT) ov er and above levels observed in animals restrained and TF tested in pr eparation for shock, and (c) basal CORT replacement in drinking water fully restored analgesia in ADX rats. These experiments demonstrate th at basal CORT, rather than adrenomedullary substances, is critical to the expression of analgesia. The function of CORT here is not linked t o a shock-induced surge of the steroid. CORT appears to play a permiss ive role in the expression of analgesia. Potential effects of the abse nce of corticosteroids on neurotransmitter biosynthesis important in a nalgesia production are discussed.