Endocrine Abstracts (2004) 7 P152

Nephrogenic diabetes insipidus in the mouse does not deplete vasopressin neurons or activate oxytocin neurons

JF Morris, MJ Epton & D Jenkins

Department of Human Anatomy and Genetics, University of Oxford, Oxford, UK.

Hereditary nephrogenic diabetes (di/di) in mice results from a failure of vasopressin (VP)action caused by overactive renal cAMP phosphodiesterase activity. The adult animals pass large amounts of dilute (100 mOsm per kg) urine and have hyperosmotic plasma (40 mOsm per kg greater than wild-type). Their osmotic status is therefore similar to that in Brattleboro rats in which both VP and oxytocin (OT) neurons are hyperactive and the neural lobe is depleted of both OT and VP. The experiments aimed to determine whether hyperosmolality stimulated both VP and OT neurons in the mouse.

Mice aged about 1 year were terminally anaesthetised; cardiac blood was taken for assay; the animals were fixed by perfusion and immuno-confocal and -electron microscopy used to assess the magnocellular neurons and neural lobe. VP neuron size was increased by 73% in the supraoptic nucleus and 42% in the paraventricular nucleus; oxytocin neurons were not significantly altered in size. Both vasopressin and oxytocin neurons were replete with neurosecretory vesicles in both the hypothalamus and neural lobe. As expected, plasma [VP] is increased 3-4 fold in di/di mice (Stern et al., 1982), but plasma [OT] was not significantly different in di/di and wild-type mice.

The data reveal two main points: despite the severe and chronic diabetes insipidus the VP neurons can more than keep up with the increased VP secretion which occurs; and, unlike in the rat, OT cells do not appear to be activated by the osmotic stress.

Stern P et al. (1982) Kidney International 21:266.

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