Multiple episodes of sodium depletion in the rat: a remodeling of the electrical properties of median preoptic nucleus neurons

In rat brain, the detection and integration of chemosensory and neural signals are achieved, inter alia , by the median preoptic nucleus ( MnPO ) during a disturbance of the hydromineral balance. This is allowed through the presence of the sodium ( Na + ) sensor neurons. Interestingly, enkephalins and mu‐opioid receptors ( μ‐ORs ) are known for their role in ingestive behaviors and have previously been shown to regulate the excitability of MnPO neurons following a single Na + depletion. However, little is known about the role of these μ‐ORs in the response enhancement following repeated Na + challenge. Therefore, we used whole‐cell recordings in acute brain slices to determine neuronal plasticity in the electrical properties of the MnPO Na + sensor‐specific neuronal population following multiple Na + depletions. Our results show that the population of Na + sensor neurons was represented by 80% of MnPO neurons after a single Na + depletion and was reduced after three Na + depletions. Interestingly, the subpopulation of Na + sensors responding to D‐Ala 2 ,N‐MePhe 4 ,Gly‐ol‐enkephalin ( DAMGO ), a specific μ‐OR agonist, represented 11% of MnPO neurons after a single Na + depletion and the population doubled after three Na + depletions. Moreover, Na + sensor neurons displayed modifications in the discharge pattern distribution and shape of calcium action potentials after three Na + depletions but these changes did not occur in Na + sensors responding to DAMGO . Thus, the reinforced μ‐OR functionality in Na + sensors might take place to control the neuronal hyperexcitability and this plasticity in opioid‐sensitive and Na + detection MnPO networks might sustain the enhanced salt ingestion induced by repeated exposure to Na + depletion.