CRF triggers the CNS release of TRH in stress-induced changes in gastric emptying

Stress elicited by exposure to cold induces an increase of gastric emptying (GE) and intestinal transit of a caloric meal in mice and the release of corticotropin-releasing factor (CRF) and thyrotropin-releasing hormone (TRH) in the central nervous system (CNS). The present study proposed 1) to compare in mice the central effects of TRH, CRF, and cold-exposure stress on GE and intestinal transit of a caloric test meal consisting of 0.5 ml of reconstituted milk marked with 51Cr-labeled sodium chromate, and 2) using CRF and TRH antisera to determine whether TRH and CRF act in cascade or independently. The intracerebroventricular (icv) injection of TRH (0.5 microgram/kg) and CRF (1 microgram/kg), as well as cold stress, significantly increased GE, whereas 10-fold higher doses injected intraperitoneally were ineffective. The effect of cold stress on GE was abolished by prior icv injection of both CRF and TRH antisera. The effect of TRH was not blocked by CRF antiserum, but TRH antiserum suppressed the increase in GE induced by CRF. Moreover, both CRF and TRH antisera abolished changes in the rate of GE induced by exogenous CRF and TRH injection, respectively, therefore demonstrating the specific efficiency of immunoneutralization. CRF and cold stress both induced an increase in the rate of intestinal transit, while TRH had no effect. Antibodies to CRF prevented the intestinal stimulatory effect induced by CRF and cold stress. In contrast, antibodies to TRH were unable to antagonize either CRF or cold-stress induced increase in the rate of intestinal transit.(ABSTRACT TRUNCATED AT 250 WORDS)