A functional ultrastructural assay was used to determine the response of corticotropin releasing hormone (CRH) neurosecretory cells to short-term stress. Depletion of neurosecretory vesicles from axonal swellings in the external zone of the rat median eminence was used as a measure of functional activity. One hour of immobilization or 5 h of insulin-induced hypoglycemia caused marked depletion of vesicles from the vasopressin (VP)-containing CRH axons, but had no effect on the VP-deficient subpopulation of CRH axons. Injection of colchicine (100 µg) into the lateral ventricle also resulted in selective depletion of vesicles from the VP-containing subpopulation over the course of 5 h, with no depletion from the VP-deficient axons. By 24 h after injection of 100 µg colchicine, however, both the VP-containing and the VP-deficient axons were severely depleted of neurosecretory vesicles. These data demonstrate for the first time that the CRH neurosecretory system contains functionally distinct components, and that the VP secreting component may specifically mediate the ACTH response to short-term stress.

Keywords:
Stress, Vasopressin, CRH, Coexistence, Subpopulations, Paraventricular nucleus, Median eminence, Electron microscopy, Immunocytochemistry
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© 1989 S. Karger AG, Basel
1989
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