CHRONIC HYPONATREMIA REDUCES SURVIVAL OF MAGNOCELLULAR VASOPRESSIN AND OXYTOCIN NEURONS AFTER AXONAL INJURY

Axonal injury to hypothalamic magnocellular vasopressin (AVP) and oxyt ocin (OT) neurons causes degeneration of a substantial subpopulation o f these neurons. In this study, we investigated the influence of osmol ality on this injury-induced cell death. Normonatremic, chronically hy pernatremic, and chronically hyponatremic rats received pituitary stal k compression (SC), which causes degeneration of AVP and OT terminals in the neurohypophysis. Twenty-one days after SC, rats were perfused a nd hypothalami were serially sectioned and alternately stained for AVP -neurophysin and OT-neurophysin immunoreactivities. Normonatremic and hypernatremic rats exhibited a triphasic pattern of water intake after SC, with peak intakes 3 times higher than those exhibited by sham-ope rated normonatremic rats. In contrast, hyponatremic SC rats exhibited peak water intakes of 600 ml/24 hr, similar to 9-10 times the water in takes of sham-operated normonatremic rats. In normonatremic rats, SC c aused degeneration of 65% of the AVP neuron population in the SON and 73% in the PVN, but only 31% of the OT neuron population in the SON an d 35% in the PVN. Similar results were found in hypernatremic rats aft er SC. However, in hyponatremic rats SC caused degeneration of 97% of the AVP neuron population in the SON and 93% in the PVN, and 90% of th e OT neuron population in the SON and 84% in the PVN. Our results, the refore, demonstrate that injury-induced degeneration of magnocellular AVP and OT neurons is markedly exacerbated by chronic hypo-osmolar con ditions, but neuronal survival is not enhanced by chronic hyperosmolar conditions.