Corticotropin-releasing factor (CRF-41) and arginine vasopressin (AVP) are the two major factors that regulate adrenocorticotropic hormone (ACTH) secretion. The two neurohormones are co-localized in the parvocellular neurons of the paraventricular nuclei (PVN) of the hypothalamus and are capable of potentiating each others' action on freshly excised anterior pituitary fragments or cells in vitro. Transection of all axons entering the medial basal hypothalamus from anterior and lateral directions blocks ACTH release induced by either adrenalectomy or ether-surgery stress. Adrenalectomy-induced ACTH release is almost completely suppressed by a long-term lesion of the PVN. Stress-induced ACTH release is blocked for only a few days after PVN lesion and the pituitary-adrenal response to ether-surgery stress returns to a large extent by a few weeks after PVN lesioning. This remarkable plasticity can be observed also in the homozygous Brattleboro rat, therefore it is not dependent on mediation by AVP. When parvocellular CRF-41- and AVP-containing cells are present, and the anterior lobe ACTH cells are desensitized to the stimulating effects of AVP, the ACTH response to haemorrhage and immobilization is markedly decreased. This indicates that AVP may partially mediate ACTH release under normal conditions. The hypothalamic control of the pituitary-adrenocortical system has a remarkable degree of redundancy which may compensate, at least under stressful conditions, for disruption of the function of CRF-41-containing cells of the paraventricular nucleus, the major source of CRF-41 in the stalk-median eminence.
|Pages (from-to)||43-51; discussion 51-53|
|Journal||Ciba Foundation symposium|
|Publication status||Published - 1992|
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