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AJP - Regulatory, Integrative and Comparative Physiology, Vol 261, Issue 1 38-R43, Copyright © 1991 by American Physiological Society
ARTICLES |
D. L. Helmreich, E. Thiels, A. F. Sved, J. G. Verbalis and E. M. Stricker
Department of Behavioral Neuroscience, University of Pittsburgh, Pennsylvania 15260.
Recent reports indicate that in male rats dehydration, LiCl, and cholecystokinin (CCK) each stimulate pituitary oxytocin (OT) secretion and also decrease gastric emptying and motility. In contrast, the present experiments demonstrate that nipple attachment and sucking by pups, a well-known stimulus for neurohypophysial secretion of OT, did not decrease gastric motility in lactating rats. Moreover, systemic injection of naloxone, which is known to potentiate the inhibitory effects of LiCl and CCK on gastric motility in male rats, had no effect on gastric motility of lactating rats while nursing. These data indicate that pituitary OT secretion from magnocellular neurons is not invariably linked to decreased gastric motility in rats. As such, our results support previous findings that inhibition of gastric motility is not secondary to the pituitary secretion of OT but allow a possible role for parvocellular oxytocinergic neurons that project from the hypothalamic paraventricular nucleus to the brain stem in the control of gastric function.
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