Normal, intact rats generally show transient elevations of pituitary-adrenal hormones in response to acute stress. The immediate hypersecretion, followed by return to baseline levels after approximately 2 h, is believed to be due to CRF of median eminence origin (ME-CRF). Lesioned rats, on the other hand, do not usually exhibit an immediate response, but under certain conditions show a delayed hypersecretion of pituitary-adrenal hormones 2–4 h later. From our previous studies it has been demonstrated that the delayed response of lesioned rats is due to release of tissue-CRF. To examine the relationship between ME-CRF and tissue-CRF, groups of lesioned animals were subjected to the stress of plasma injection or laparotomy. Both stimuli produced a delayed hypersecretion of corticosterone 2–8 h later. When, however, ME-CRF or ACTH was administered at the time of application of the stress, the expected delayed response was significantly suppressed and plasma corticosterone levels approached baseline values. To determine how the delayed response was suppressed, one group of lesioned-hypophysectomized donor rats was subjected to laparotomy stress and 5 h later the blood from these animals was assayed for tissue-CRF. Another group of lesioned-hypophysectomized rats was not only subjected to the laparotomy stress but also injected with ACTH at the same time and then tested for blood CRF activity 5 h later. Prior administration of ACTH caused a significant reduction in the tissue-CRF levels in the peripheral blood. Therefore it appears that suppression of the delayed response by ME extract

Keywords:
CRF assay, Hypothalamic lesion, Corticosterone
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© 1974 S. Karger AG, Basel
1973
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