CHOLECYSTOKININ BLOCKADE OF EMOTIONAL STRESS-INDUCED AND CRF-INDUCED COLONIC MOTOR ALTERATIONS IN RATS - ROLE OF THE AMYGDALA

Intracerebroventricular (i.c.v.) injection of corticotropin-releasing factor (CRF) and emotional stress (ES) induce stimulation of colonic m otility in rats, an effect blocked by i.c.v. injection of CCK-8s. This study examined in rats the contribution of the central nucleus of the amygdala (CA) in the blocking effect of CCK-8s on ES and CRF-induced colonic hypermotility. CRF (500 ng/kg, i.c.v.) induced a 73.5% increas e in colonic spike burst frequency. Bilateral infusions of 1, 5, 10 an d 20 ng/kg of CCK-8s in the CA region 10 min prior to CRF i.c.v. injec tion reduced, in a dose related manner, the CRF-induced stimulation of colonic motility. A 109% increase in colonic spike burst frequency wa s observed in rats placed in a test cage in which they had previously received electric footshocks (ES). CCK-8s and A-71623, a selective CCK -A receptor agonist, (10, 25 and 50 ng/kg) infused bilaterally into th e CA, 30 min before ES, significantly reduced this stimulatory effect, while CCK-4 and A-63387, a selective CCK-B receptor agonist (10, 25 a nd 50 ng/kg), had no effect on such a response. CA lesions by ibotenic acid did not affect ES-induced increase in colonic spike activity. Ho wever, CCK-8s (50 ng/kg) microinfused into CA lesioned rats was unable to block the ES-induced stimulation of colonic motility, while CCK-8s i.c.v. injected (100 ng/kg) is still active on the colonic response t o ES. These results suggest that CA is a site of interaction of CCK-8s with CRF to block the colonic response to stress and that these effec ts involve the CCK-A receptor subtype. Furthermore, CA is not a brain structure involved in stress-induced stimulation of colonic motility.