Several lines of evidence suggest that centrally released oxytocin (OT) may act in the hypothalamic ventromedial nucleus (VMN) to facilitate sexual behavior in female rats primed with estradiol and progesterone. The present experiment used a marker of neuronal activation, expression of the transcription factor FOS, to locate OT neurons activated during sexual behavior. Sexual behavior significantly increased the percentage of OT neurons in the hypothalamic paraventricular nucleus (PVN) expressing FOS in rats treated with estradiol and progesterone, compared to hormone-treated, nonmated controls. The OT neurons colabelled with FOS immunoreactivity were found in regions of the PVN, but not in the supraoptic nucleus. As reported by others, FOS expression also was induced in the preoptic area and the VMN. Taken together with other evidence, the results are consistent with the hypothesis that endogenous OT is involved in female sexual behavior, and suggest that the source of oxytocinergic innervation to the oxytocin receptors in the VMN may be neurons in the PVN. Interestingly, FOS expression in the VMN occurred in cells in the vicinity of OT fibers.
In these experiments we examined the effects on gastric motility of cholecystokinin, LiCl, hypertonic NaCl solution, gastric distension, and intraduodenal glucose loads, five dissimilar treatments known to reduce food intake in rats. In addition, we investigated whether any observed effects were dependent on the afferent vagus nerve by pretreating subjects with the neurotoxin capsaicin. Each of the five treatments virtually eliminated the gastric contractions seen after rats had consumed a large meal of chow; these effects were rapid in onset and continued for up to 30 min. The inhibitory effects of cholecystokinin and gastric distension were eliminated by pretreatment with capsaicin, whereas the effects of the other treatments were attenuated only slightly or not at all. Because most of these treatments have been shown to stimulate pituitary oxytocin secretion in rats as well as to inhibit food intake and gastric motility, these results are consistent with the hypothesis that the hypothalamic paraventricular nucleus is a site at which information is integrated in the coordinated control of food intake, gastric function, and neuroendocrine secretion.
Systemic administration of cholecystokinin (CCK) or LiCl inhibits gastric motility and food intake in rats. Brain stem-projecting oxytocin (OT) neurons in the hypothalamic paraventricular nucleus (PVN) have been proposed to mediate the inhibitory effects of CCK and LiCl on gastric motility and food intake. In the present studies, we found that basal gastric motility was elevated in rats 12-20 h after knife-cut lesions of the PVN; however, this effect disappeared 3 days later. Furthermore, CCK and LiCl inhibited gastric motility at 12-20 h, 3 days, and 3 wk after PVN lesions, although their effects were blunted. Injection of the local anesthetic lidocaine into the PVN had effects similar to acute PVN lesions. In rats with PVN lesions, the inhibitory effects of CCK and LiCl on food intake were indistinguishable from those in sham-lesioned rats. We conclude that the PVN tonically inhibits gastric motility and that it participates in, but is not essential for, the inhibitory effects of CCK and LiCl on gastric motility and food intake in rats.
Several diverse treatments that stimulate pituitary secretion of oxytocin (OT) in rats produce a parallel inhibition of gastric motility and food intake. The present experiments demonstrate that injection of hypertonic saline (HS) is another such treatment. Systemic administration of large doses of OT had no effect on gastric motility. Lesions within the region anteroventral to the third ventricle (AV3V region) severely impaired the drinking response to HS without affecting its inhibition of either gastric motility or food intake. These and other results suggest that despite the close association of pituitary secretion of OT with inhibition of both gastric motility and food intake in intact animals after HS administration, these effects may be dissociated by lesions within the AV3V region. Consequently, osmosensitive cells located within the periventricular tissue of the rostral AV3V region, which are critical for the stimulation of thirst and pituitary OT secretion after systemic injection of HS, do not appear to be essential for the parallel inhibition of gastric motility and food intake produced by this treatment in rats.
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