Expression of Mineralocorticoid and Glucocorticoid receptors in Pre‐autonomic Neurons of the Rat Paraventricular Nucleus

Abstract

Plasma aldosterone levels that are inappropriately high for the sodium intake increases sympathetic nervous system (SNS) activity and the hypertension and increased SNS activity in experimental mineralocorticoid‐salt excess is abrogated by lesions of the paraventricular nucleus (PVN) or antagonists of the mineralocorticoid receptors (MR). It is uncertain whether physiological concentrations of aldosterone bind MR in the PVN; corticosterone and cortisol bind both MR and glucocorticoid (GR) receptors at physiological concentrations and MR and GR influence each other at transcriptional and functional levels. The retrograde tracer Fast Blue was injected into the IMLCC at the level of T4 and T10 of spinal cord after laminectomy to locate preautonomic neurons in the PVN. Immunofluorescent histochemistry was done in frozen modified STF‐fixed brains using specific anti‐bodies against the MR and GR to determine colocalization of these two receptors within pre‐autonomic neurons. Three different pseudo‐colors were assigned by Image‐Pro for better visualization. Expression of GR and MR varied in different parts of the PVN. Most colocalization was in mid‐PVN parvocellular neurons. Very few magnocellular pre‐autonomic neurons were found to express GR and/or MR. Adrenocortical steroids could have direct effects on sympathetic activity by binding MR and/or GR in pre‐autonomic neurons of the mid‐PVN. This limited area of expression may explain the inconsistent results of studies on the effect of PVN microinjections of MR and GR agonists and antagonists on sympathetic drive.Grant Funding Source: VA BLRDB‐ORD 1018X007080, NIH/HLBI RO1HL0272, and NIH/NCRR COBRE (Center for Psychiatric Neuroscience)