A CELL-SPECIFIC ROLE FOR THE ADRENAL-GLAND IN REGULATING CRH MESSENGER-RNA LEVELS IN RAT HYPOTHALAMIC NEUROSECRETORY NEURONS AFTER CELLULAR DEHYDRATION

In the rat, the cellular dehydration induced by water deprivation rapidly increases CRH mRNA in magnocellular neurosecretory neurons, but gradually reduces mRNA levels in hypothalamic paraventricular parvicellular neurosecretory neurons. Using in situ hybridization we investigated a possible role for corticosterone as a mediator of the effects of water deprivation on the levels of CRH mRNA in the paraventricular and supraoptic nuclei. Following adrenalectomy and water deprivation, the reduction of CRH mRNA in the medial parvicellular part of the paraventricular nucleus was inhibited. However, replacement of low-doses of corticosterone to dehydrated adrenalectomized animals was not sufficient to reduce parvicellular CRH mRNA levels to those seen in intact dehydrated animals. Neither adrenalectomy nor corticosterone replacement had any effect on the increased CRH mRNA levels in magnocellular neurosecretory neurons. We conclude that an intact adrenal gland is required for the decreased levels of CRH mRNA seen during water deprivation in parvicellular paraventricular neurosecretory neurons, but not magnocellular neurosecretory neurons. These effects may be mediated by the increased corticosterone secretion seen during water deprivation.