Involvement of brain CCK in the adaptation of gut motility to digestive status and stress: a review.

Cholecystokinin is involved at both central and peripheral level in the control of gut motility. At CNS level, CCK8 appears to play a major role in the adaptation of duodeno-jejunal motility to the postprandial state, ie the disruption of the migrating motor complex. CCK8 microinjected into the ventro-medial nucleus of the hypothalamus (VLH) induces a fed-like pattern not reproduced by similar administration into the hypothalamus. Furthermore, CCKA antagonists such as devazepide injected into the VMH just prior to the meal shortens the duration of the postprandial pattern of activity, an effect not reproduced by similar injection into the LH. Similarly the colonic motor activation observed after feeding is suppressed by devazepide injected into the VMH in rats. In addition, icv administration of CCKA but not CCKB receptor antagonist prevents meal- and CCK8-induced colonic hyperkinesia in dogs. In rats, emotional stress is associated with an increase in colonic motility related to the central release of CRF. We have shown that CCK8 injected centrally, at a lower dose than that producing an increase in colonic motility, is able to prevent stress-induced colonic motor alteration.