1. In many mammals, severe dehydration is known to cause exhaustion of the vasopressin content of the neural lobe. Here, we have examined the physiological state of the neurohypophysis of the jerboa Jaculus orientalis, a rodent inhabitant of a semi-desert climate. 2. Isolated neurohypophyses and neurosecretory nerve endings were perfused in vitro and vasopressin and oxytocin release were determined by radioimmunoassay. 3. Electrical stimulation of the neurohypophysis with bursts of pulses mimicking the activity of hypersecreting neuroendocrine neurones induced similar increases of secretion in both control animals and animals dehydrated for up to 2 months. Neurohormone release was greatly potentiated when the bursts of pulses were separated by silent intervals. 4. Prolonged stimulation of neurohypophyses from both control and dehydrated animals induced a sustained increase of vasopressin release; in contrast, oxytocin release under similar conditions showed a biphasic secretory pattern consisting of a transient increase that subsequently decreased to a steady level whose amplitude was similar to that for vasopressin. 5. K(+)-induced secretion was largely inhibited by the Ca2+ channel blockers nicardipine and omega-conotoxin, suggesting that in this neurosecretory system both L- and N-type calcium channels play a major role in stimulus-secretion coupling. Depolarization of isolated nerve endings using a fast-flow perifusion system showed that there was no difference in the amplitude and the time course of the secretory response in dehydrated and hydrated animals. 6. The results demonstrate that, despite the climatic conditions in which the jerboas live, their neural lobes retain the capacity to release, upon depolarization of the plasma membrane of the nerve endings, large amounts of neurohormone. It is concluded that the neurohypophyseal peptidergic release system in the dehydrated jerboa functions adequately even under extreme environmental stress.
Stimulation of Central and Systemic Oxytocin Release by Histamine in the Paraventricular Hypothalamic Nucleus: Evidence for an Interaction with Norepinephrine*