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Expression in Magnocellular Vasopressin Neurons Requires the Lamina Terminalis
1 Department of Physiology and Biophysics, University of Colorado Health Sciences Center, Denver, Colorado, USA
2 Department of Psychology and Pharmacology, University of Iowa, Iowa City, Iowa, USA
* To whom correspondence should be addressed. E-mail: celia.sladek{at}uchsc.edu.
Estrogen receptor-
(ER-) expression in rat magnocellular vasopressin (VP) neurons of the supraoptic (SON) and paraventricular nuclei (PVN) becomes undetectable following 72h of 2% NaCl consumption. To test the hypothesis that osmosensitive mechanisms originating in the region of the organum vasculosum lamina terminalis (OVLT) control ER- expression in SON and PVN, animals were water deprived following electrolytic lesions of the area anterior and ventral to the 3rd ventricle (AV3V). Such lesions prevent osmotic stimulation of VP release. 4wks post-surgery, male rats [lesioned (n=16) or sham (n=14)] were water deprived for 48h 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 to the sham-hydrated rats (pOsm: 304±1 vs 318±2 mOsm/kg H20, 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 in 6 of 8 AV3V-dehydrated rats despite significant increases in pOsm in both groups (AV3V-hydrated: 312±2; AV3V-dehydrated: 380±10; 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 in spite of the elevated pOsm. In AV3V-dehydrated rats, it was significantly less than in sham-dehydrated animals, but was significantly increased compared to the sham-hydrated group. This could reflect activation by non-osmotic parameters that do not inhibit ER- expression. These data support the hypothesis that inhibition of ER- expression in SON by osmotic stimulation is mediated by osmoreceptive neurons in the lamina terminalis.
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