title: Chronic hyponatremia reduces survival of magnocellular vasopressin and oxytocin neurons after axonal injury.
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 9-10 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.
authors.affiliation: Department of Medicine, University of Pittsburgh, Pennsylvania 15261, USA.
authors.forename: J
authors.initials: J
authors.lastname: Dohanics
authors.forename: G E
authors.initials: GE
authors.lastname: Hoffman
authors.forename: J G
authors.initials: JG
authors.lastname: Verbalis
mesh_terms: D000818:Animals; D001369:Axons / Q000502:physiology*; D002452:Cell Count; D016923:Cell Death / Q000502:physiology; D002470:Cell Survival / Q000502:physiology; D003894:Deamino Arginine Vasopressin / Q000494:pharmacology; D004326:Drinking; D006955:Hypernatremia / Q000139:chemically induced / Q000503:physiopathology; D007010:Hyponatremia / Q000139:chemically induced / Q000503:physiopathology*; D008297:Male; D009410:Nerve Degeneration / Q000502:physiology; D009474:Neurons / Q000737:chemistry / Q000166:cytology* / Q000648:ultrastructure; D010121:Oxytocin / Q000032:analysis; D051381:Rats; D017207:Rats, Sprague-Dawley; D012964:Sodium / Q000097:blood; D012965:Sodium Chloride / Q000494:pharmacology; D013997:Time Factors; D014667:Vasopressins / Q000032:analysis
chemical_list: D014667:Vasopressins; D012965:Sodium Chloride; D010121:Oxytocin; D012964:Sodium; D003894:Deamino Arginine Vasopressin