Abstract
Water deprivation (WD) represents a physiological challenge that results in the sustained release of vasopressin (AVP) that is inhibited by water intake. We and others have previously shown that WD enhances glutamate signaling in AVP magnocellular neurosecretory cells (MNCs). In this study, we tested the hypothesis that WD has profound effects on GABA neurotransmission as well. One mechanism that could alter GABAergic neurotransmission in AVP MNCs is through the chloride extruder K+/Cl− cotransporter (KCC2). Changes in the expression and function of KCC2 could influence the intracellular concentration of Cl− and alter the synaptic inhibitory tone of MNCs located in the supraoptic (SON) and paraventricular nuclei (PVN) of the hypothalamus. Using laser capture microdissection (LCM),7–10 quick immunolabled AVP cells were harvested from the SON and PVN of euhydrated and 48 h WD adult male rats and RT‐PCR was used to test for changes in KCC2 message. We observed a significant elevation in KCC2 mRNA expression in AVP cells of the SON (WD 2.5 ± 0.52; Control 1.0 ± 0.06, p<0.05) but not in the PVN (WD 3.5 ± 1.7; Control 1.0 ± 0.1). Immunofluorescence demonstrated the colocalization of KCC2 and AVP in the SON. Increased expression of KCC2 could be associated with decreased intracellular Cl− in AVP neurons in the SON, thereby serving to maintain or enhance the inhibitory tone of AVP neurons in the SON but not the PVN during WD. HL62569
Published Version
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