@article {Dohanics2373, author = {J Dohanics and GE Hoffman and JG Verbalis}, title = {Chronic hyponatremia reduces survival of magnocellular vasopressin and oxytocin neurons after axonal injury}, volume = {16}, number = {7}, pages = {2373--2380}, year = {1996}, doi = {10.1523/JNEUROSCI.16-07-02373.1996}, publisher = {Society for Neuroscience}, abstract = {Axonal injury to hypothalamic magnocellular vasopressin (AVP) and oxytocin (OT) neurons causes degeneration of a substantial subpopulation of these neurons. In this study, we investigated the influence of osmolality on this injury-induced cell death. Normonatremic, chronically hypernatremic, and chronically hyponatremic rats received pituitary stalk compression (SC), which causes degeneration of AVP and OT terminals in the neurohypophysis. Twenty-one days after SC, rats were perfused and 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-operated normonatremic rats. In contrast, hyponatremic SC rats exhibited peak water intakes of 600 ml/24 hr, approximately 9{\textendash}10 times the water intakes of sham-operated normonatremic rats. In normonatremic rats, SC caused 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 and 35\% in the PVN. Similar results were found in hypernatremic rats after 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 the OT neuron population in the SON and 84\% in the PVN. Our results, therefore, demonstrate that injury-induced degeneration of magnocellular AVP and OT neurons is markedly exacerbated by chronic hypo-osmolar conditions, but neuronal survival is not enhanced by chronic hyperosmolar conditions.}, issn = {0270-6474}, URL = {https://www.jneurosci.org/content/16/7/2373}, eprint = {https://www.jneurosci.org/content/16/7/2373.full.pdf}, journal = {Journal of Neuroscience} }