PLASMA CRH RESPONSE TO WATER IMMERSION-RESTRAINT STRESS IN RATS BEARING A HYPOTHALAMIC KNIFE CUT

We reported earlier that the plasma level of corticotropin-releasing h ormone (CRH) remained high 120 min after the onset of such strong sust ained stress as ether-laparotomy or water immersion-restraint, which r eflected the persistent secretion of CRH from the hypothalamic median eminence (ME). We investigated the change in plasma CRH during water i mmersion-restraint stress in rats bearing an anterolateral cut around the medial basal hypothalamus (MBH) which cuts the CRH neurons from th e PVN to the ME. Concentrations of CRH in the hypothalamus, extrahypot halamic tissues and peripheral blood were measured by radioimmunoassay . Plasma ACTH was measured with an immunoradiometric assay kit. Plasma baseline ACTH and CRH concentrations did not differ significantly in the sham vs. cut groups. At 120 min after the onset of stress, plasma ACTH concentrations were definitely higher in both groups. In the cut group, plasma CRH at 120 min after stress did not differ significantly from the baseline level, whereas plasma CRH at 120 min was definitely higher in the sham group. Baseline CRH concentrations in the ME did n ot differ greatly in the two groups. CRH concentrations in the ME of b oth groups had decreased appreciably 120 min after the onset of stress as compared with baseline CRH, and the CRH decrease was greater in th e cut group than in the sham group. CRH in the neurointermediate lobe (NIL) and adrenal gland of both groups showed no significant change at 120 min, compared with the control. These findings confirm that the c ontinuous CRH increase in plasma during sustained stress is derived ma inly from the hypothalamus. It is possible that the ACTH increase at 1 20 min in the cut group depends not only on the secretion of pooled CR H in the ME but also on other ACTH-stimulating factors from peripheral tissues.