Olfactory bulbectomy increases vasopressin, but not corticotropin-releasing hormone, content in the external layer of the median eminence of male rats.

Removal of the olfactory bulbs results in numerous physiological and behavioral changes in rats. The most frequent and characteristic change is an abnormally high level of corticosterone in the blood, possibly due to changes in the activity of the hypothalamic neurons which synthesize corticotrophin-releasing hormone (CRH). Some of these neurons also synthesize vasopressin (AVP). They are located in the parvocellular part of the paraventricular nucleus of the hypothalamus, which projects into the external layer of the median eminence. We investigated whether there was such a change in activity by studying the synthesis and storage activity of CRH neurons in bulbectomized rats. CRH and AVP axon terminals in frozen sections of the external layer of the median eminence were labeled by immunofluorescence techniques and the degree of labeling was analyzed semi quantitatively. There was no difference in the area or intensity of CRH-labeling in control and bulbectomized rats. However, a significantly larger area was stained for AVP in the bulbectomized than in control rats. We also used in situ hybridization, with single- and double-labeling, to study the effects of bulbectomy on expression of the genes encoding CRH and AVP. No significant difference was found in the levels of mRNA for CRH and the number of CRH+/AVP+ cell bodies was similar in the parvocellular part of the paraventricular nucleus in bulbectomized and normal rats. Our results suggest that the hypothalamo-pituitary-adrenal (HPA) axis changes observed after olfactory bulbectomy may be due to plastic changes in hypothalamic CRH neurons, resulting in greater storage of increased AVP in CRH neurosecretory nerve terminals in the external layer of the median eminence.