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THIRST AND VOLUME, ELECTROLYTE HOMEOSTASIS
expression in magnocellular vasopressin neurons requires lamina terminalis
1Department of Physiology and Biophysics, University of Colorado Health Science Center, Denver, Colorado 80262 and 2Departments of Psychology and Pharmacology, University of Iowa, Iowa City, Iowa 52242
Submitted 21 August 2003 ; accepted in final form 4 November 2003
Estrogen receptor-
(ER-) expression in rat magnocellular vasopressin (VP) neurons of the supraoptic and paraventricular nuclei (SON and PVN, respectively) becomes undetectable after 72 h of 2% NaCl consumption. To test the hypothesis that osmosensitive mechanisms that originate in the region of the organum vasculosum lamina terminalis (OVLT) control ER- expression in the SON and PVN, animals were water deprived after electrolytic lesions were performed on the area anterior to the ventral third ventricle (AV3V). Such lesions prevent osmotic stimulation of VP release. Four weeks after surgery, male rats [lesioned (n = 16) or sham (n = 14)] were water deprived for 48 h or allowed water ad libitum. Water deprivation eliminated ER--immunoreactivity (-ir) in SON and magnocellular PVN of sham-lesioned animals. Fos-ir was evident in these neurons, and plasma osmolality (Posm) and hematocrit (Ht) were significantly elevated compared with the sham-hydrated rats (Posm, 304 ± 1 vs. 318 ± 2 mosmol/kgH2O; P < 0.001; Ht, 49.6 ± 0.6 vs. 55.0 ± 0.9%; P < 0.001). ER- expression was comparable in sham-hydrated, AV3V-hydrated, and 6 of 8 AV3V-dehydrated rats despite significant increases in Posm in both groups (AV3V hydrated, 312 ± 2; AV3V dehydrated, 380 ± 10 mosmol/kgH2O; P < 0.001). OVLT was not ablated in the AV3V-dehydrated rats in which ER- was depleted. Fos-ir was low or undetectable in SON in the AV3V-hydrated animals despite elevated Posm values. In AV3V-dehydrated rats, Fos-ir was significantly less than in sham-dehydrated animals but was significantly increased compared with the sham-hydrated group. This could reflect activation by nonosmotic parameters that do not inhibit ER- expression. These data support the hypothesis that inhibition of ER- expression in the SON by osmotic stimulation is mediated by osmoreceptive neurons in the lamina terminalis.
anteroventral third ventricle paraventricular nucleus; organum vasculosum; oxytocin; water deprivation; supraoptic nucleus
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