Citation

Ferris CF, Pilapil CG, Hayden‐Hixson D, Wiley RG, Koh ET. J. Neuroendocrinol. 1992; 4(2): 193-205.

Copyright

(Copyright © 1992, John Wiley and Sons)

DOI

10.1111/j.1365-2826.1992.tb00159.x

PMID

unavailable

Abstract

The present study was done to determine whether the vasopressinergic neurons in the hypothalamus controlling flank marking behavior are distinct from the magnocellular neurons comprising the hypothalamo‐neurohypophysial system. Animals were either hypophysectomized or injected with a suicide transport lectin, volkensin, into the neurohypophysis. Both procedures resulted in a pronounced loss of vasopressin‐immunoreactive perikarya throughout the hypothalamus concomitant with increases in water intake and urine output and decreases in circulating levels of vasopressin. The loss of the hypothalamo‐neurohypophysial system was most pronounced in volkensin‐treated animals that presented with frank diabetes insipidus and exceedingly low levels of plasma vasopressin. However, the vasopressinergic fibers and magnocellular neurons in and around the anterior hypothalamus implicated in the control of flank marking survived the volkensin treatment. Volkensin‐treated animals exhibited levels of flank marking typical of untreated animals. These data suggest the presence of anatomically and functionally distinct populations of vasopressinergic magnocellular neurons in the hypothalamus of the golden hamster. Copyright © 1992, Wiley Blackwell. All rights reserved

Language: en

Keywords

female; article; controlled study; behavior; nonhuman; animal experiment; diabetes insipidus; animal; vasopressin; fluid intake; animal tissue; hypothalamus; hypothalamus hypophysis system; urine volume; nerve cell necrosis; functional anatomy; anterior hypothalamus; flank marking; hypophysectomy; lectin; magnocellular nucleus; perikaryon; vasopressin blood level; vasopressin receptor; volkensin