Animal models of Central Diabetes Insipidus: Human relevance of acquired beyond hereditary syndromes and the role of oxytocin Bernal Benítez, Antonio Mahía Rodríguez, Javier Puerto Salgado, Amadeo Brattleboro rat Hereditary and traumatic diabetes insipidus Arginine vasopressin Oxytocin Water intake Urine volume Natriuresis Polydipsia Synergic hormonal effects The aim of this study was to review different animal models of Central Diabetes Insipidus, a neuro- biological syndrome characterized by the excretion of copious amounts of diluted urine (polyuria), a consequent water intake (polydipsia), and a rise in the serum sodium concentration (hypernatremia). In rodents, Central Diabetes Insipidus can be caused by genetic disorders (Brattleboro rats) but also by various traumatic/surgical interventions, including neurohypophysectomy, pituitary stalk compression, hypophysectomy, and median eminence lesions. Regardless of its etiology, Central Diabetes Insipidus affects the neuroendocrine system that secretes arginine vasopressin, a neurohormone responsible for antidiuretic functions that acts trough the renal system. However, most Central Diabetes Insipidus mod- els also show disorders in other neurobiological systems, specifically in the secretion of oxytocin, a neurohormone involved in body sodium excretion. Although the hydromineral behaviors shown by the different Central Diabetes Insipidus models have usually been considered as very similar, the present review highlights relevant differences with respect to these behaviors as a function of the individual neurobiological systems affected. Increased understand- ing of the relationship between the neuroendocrine systems involved and the associated hydromineral behaviors may allow appropriate action to be taken to correct these behavioral neuroendocrine deficits. 2023-12-19T08:19:24Z 2023-12-19T08:19:24Z 2016-04-23 journal article https://hdl.handle.net/10481/86333 http://dx.doi.org/10.1016/j.neubiorev.2016.02.023 eng http://creativecommons.org/licenses/by-nc-nd/4.0/ open access Attribution-NonCommercial-NoDerivatives 4.0 Internacional Elsevier