Postsynaptic mu-opioid receptor response in the median preoptic nucleus is altered by a systemic sodium challenge in rats.

The median preoptic nucleus (MnPO) is an integrator site for the chemosensory and neural signals induced by a perturbation in the hydromineral balance, and it is highly involved in controlling fluid and electrolyte ingestion. Here, we hypothesize that opioid peptides, previously recognized to control ingestive behaviors, may regulate the excitability of MnPO neurons and that this regulatory action may depend on the natriuric (Na(+)) status of body fluid compartments. Our results show that activation of mu-, but not delta-, opioid receptors (OR) triggered a membrane hyperpolarization by recruiting a G-protein-regulated inward-rectifier K(+) (GIRK) conductance in 41% of the neurons tested. Interestingly, 24 h Na(+) depletion strengthened this opioid-mediated control of neuronal excitability. In Na(+)-depleted animals, the neuronal population displaying the mu-OR-induced hyperpolarization expanded to 60% (Z-test, P = 0.012), whereas Na(+) repletion restored this population to the control level (39%; Z-test, P = 0.037). Among the neurons displaying mu-OR-induced hyperpolarization, Na(+) depletion specifically increased the neuronal population responsive to variation in ambient Na(+) (from 27% to 43%; Z-test, P = 0.029). In contrast, Na(+) repletion dramatically reduced the population that was unresponsive to Na(+) (from 17% to 3%; Z-test, P = 0.031). Neither the basic properties of the neurons nor the characteristics of the mu-OR-induced response were altered by the body Na(+) challenge. Our results indicate that an episode of Na(+) depletion/Na(+) repletion modifies the organization of the opioid-sensitive network of the MnPO. Such network plasticity might be related to the avid salt ingestion triggered by repeated Na(+) depletion.