The role of dopamine in the genesis of corticotropin releasing factor (CRF)‐ and emotional stress (ES)‐induced stimulation of colonic motility, as well as the mechanism of antagonistic action of cholecystokinin octapeptide (CCK‐8s) and igmesine (a σ receptor ligand, formerly JO 1784) on dopamine‐induced colonic hypermotility, have been investigated in the rat. ES and i.c.v. injection of CRF (0.5 μg kg−1) increased the frequency of colonic spike bursts by 63% and 114%, respectively. Prior i.c.v. administration of (+)‐SCH 23390 (a D1 receptor antagonist, 10 μg kg−1) significantly (P < 0.05) reduced the CRF‐ and ES‐induced increase in colonic spike burst; whereas, sulpiride (a D2 receptor antagonist, 10 μg kg−1) blocked the CRF‐induced stimulation of colonic spike bursts but had no effect on the colonic response to stress. I.c.v. injection of dopamine (100 μg kg−1), increased colonic spike burst frequency by 54%. (+)‐SKF 38393 (5 μg kg−1), a selective D1 receptor agonist, and quinpirole (5 μg kg−1), a selective D2 receptor agonist, increased colonic spike burst frequency by 71% and 70% respectively. CCK‐8s (0.1 μg kg−1) and igmesine (0.1 μg kg−1) injected i.c.v. completely prevented the stimulatory effects of dopamine, (+)‐SKF 38393 and quinpirole. Previous i.c.v. injection of devazepide, a CCKA receptor antagonist, (10 μg kg−1) antagonized the inhibitory effects of both CCK‐8s and igmesine injected i.c.v. on dopamine‐induced colonic hyperkinesia. These results show that CRF stimulates colonic motility through activation of central dopaminergic mechanisms in response to stress; furthermore, CCK‐8s inhibits dopamine‐induced colonic hyperkinesia through a mechanism involving D1 and D2 receptors. The σ receptor ligand igmesine, blocks the CRF‐ and ES‐induced colonic hyperactivity via an interaction with central CCK mechanisms.
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