A new stress model in rats produced changes in intestinal function that resemble patterns of intestinal dysfunction associated with stress in humans: small intestinal transit was inhibited, large intestinal transit was stimulated, and fecal excretion was stimulated. To evaluate the role of corticotropin-releasing factor (CRF) in mediating the effects of stress on the intestine, we studied the actions of exogenous CRF on small and large intestinal transit in the rat and characterized the effects of pharmacological blockade of CRF receptors on stress-induced intestinal dysfunction. Administration of exogenous CRF (0.3-10.0 micrograms iv or icv) resulted in dose-related inhibition of gastric emptying, inhibition of small intestinal transit, stimulation of colonic transit, and stimulation of fecal excretion. The actions of exogenous CRF mimicked the effects of stress on the motor activity of the gastrointestinal tract. Administration of alpha-helical CRF-(9-41) (50 micrograms iv or icv), an antagonist of CRF, prevented the stress-induced increase in large intestinal transit and the associated increase in fecal excretion. These data suggest that endogenous CRF may mediate stress-induced changes in colonic function.

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Continuous monitoring of the electrophysiological manifestations of GnRH pulse generator activity was achieved by radiotelemetry throughout the menstrual cycles of unrestrained rhesus monkeys. The characteristic increases in hypothalamic multiunit activity (MUA volleys) associated with each LH pulse measured in the peripheral circulation were of lower frequency during the luteal phase than in the follicular phase of the cycle. Multiunit activity volley frequency increased as functional luteolysis progressed and achieved maxima of approximately one volley per hour within the first few days of the follicular phase. Unexpectedly, a dramatic decline in pulse generator frequency was observed coincidentally with the initiation of the preovulatory LH surge. Evidence is presented to support the conclusion that this deceleration of pulse generator activity is the consequence of the preovulatory rise in plasma estrogen concentration. As reported in women, a significant reduction in GnRH pulse generator frequency was observed at night during the follicular phase, but not during the luteal phase, of the menstrual cycle.

The effect of corticotropin-releasing factor (CRF) on the hypothalamic gonadotropin-releasing hormone (GnRH) pulse generator, the central neuronal system governing pulsatile pituitary luteinizing hormone (LH) secretion, was studied electrophysiologically in 6 ovariectomized rhesus monkeys bearing bilateral arrays of recording elecrodes implanted in the mediobasal hypothalamus. ‘Volleys’ of increased multiunit activity (MUA) were recorded for 6–10 h in animals placed in primate chairs. The circulating concentrations of LH and cortisol were determined by radioimmunoassay in blood samples taken every 10 min for 3–4 h prior to the administration of CRF (200 µg, i.v.) and for 3–6 h thereafter. CRF resulted in a significant decrease in the frequency of pulse generator activity in 4 of 6 animals, a significant decrease in the duration of MUA volleys and a rise in circulating cortisol levels in all 6 monkeys. Treatment with metyrapone (30 mg/kg, i.m.), an inhibitor of adrenal steroidogenesis that prevented the CRF-induced rise in serum cortisol levels, did not reverse the inhibitory effects of CRF on the frequency or duration of MUA volleys. The opiate antagonist naloxone (0.8 mg/kg, i.v., 10 min prior to CRF followed by 0.8 mg/kg/h infusion) blocked the effects of CRF on MUA volley frequency in 2 of 3 animals, but failed to block the effect of CRF on MUA volley duration, suggesting that endogenous opioids may mediate the action of CRF on pulse generator frequency but not on duration.

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