Changes in brain CCK concentrations with peripheral CCK injections in Zucker rats

Evidence suggests that the satiety responses to peripherally administered CCK are mediated by a CNS component(s). Since CCK concentrations in the hypothalamus can change with degree of hunger, they may also be involved in the feeding response to peripherally administered CCK. Six-hr fasted rats were administered saline or 2 micrograms/kg CCK-8 and half were allowed to eat a meal. They were sacrificed after a meal or after the fast and hypothalamic content of CCK was measured by RIA. In rats injected with CCK, compared with those injected with saline, CCK concentrations were decreased in the ventromedial hypothalamus (VMH, 39 vs. 47 pg/mg tissue, p less than 0.004) and dorsomedial hypothalamus (17 vs. 21 pg/mg, p less than 0.009) and increased in the lateral hypothalamus (28 vs. 19 pg/mg, p less than 0.01). CCK concentrations in fed compared with fasted rats were higher in the VMH (47 vs. 39 pg/mg, p less than 0.002) and in obese compared with lean rats CCK concentrations were higher in the paraventricular nucleus (48 vs. 38 pg/mg, p less than 0.05), suprachiasmatic nucleus (46 vs. 34 pg/mg, p less than 0.008) and VMH (52 vs. 34 pg/mg, p less than 0.001). Since peripheral injections of CCK influenced concentrations of CCK in hypothalamic areas associated with feeding, these results provide evidence that the feeding response to peripherally injected CCK may be mediated by changes in CCK content of specific brain areas.