Brain renin angiotensin system (RAS) in stress-induced analgesia and impaired retention

Physiological stress is known to produce analgesia and memory disruption. B rain renin angiotensin system (RAS) has been reported to participate in str ess response and plays a role in the processing of sensory information. Ang iotensin receptors (AT), particularly AT(1) subtypes have been reported to be distributed in brain areas that are intimately associated with stress re sponse. The purpose of present study was to examine the modulation of AT(1) receptor in the immobilization stress and angiotensin II (AngII)-induced a nalgesia and impaired retention, and to determine whether resultant behavio ral changes involve common sensory signals. Result of present experiments s howed that immobilization stress in mice and rats, and intracerebroventricu lar (ICV) administration of AngII (10 and 20 ng) in rats produced an increa se in tail-flick latency. Similarly, post training administration of AngII or immobilization stress produced impairment of retention tested on plus-ma ze learning and on passive avoidance step-down task. Both these responses w ere sensitive to reversal by prior treatment with losartan (10 and 20 mg/kg ), an AT(1) AngII receptor antagonist. On the other hand, naloxone, an opia te antagonist preferentially attenuated the stress and AngII-induced analge sia and retention deficit induced by immobilization stress, but failed to r everse the AngII induced retention deficit. These results suggest immobiliz ation stress-induced analgesia and impaired retention involves the particip ation of brain RAS. Further, failure of naloxone to reverse AngII-induced r etention impairment shows, AngII-induced behavioral changes are under contr ol of different sensory inputs. (C) 1999 Elsevier Science Inc. All rights r eserved.