Osmotic activation of neurohypophysial hormone release in rabbits with hypothalamic islands

Abstract

Electroencephalographic (EEG) changes in response to elevations in the osmolarity of blood have been correlated in earlier studies with the release of both antidiuretic hormone and oxytocin from the neurohypophysis. To determine whether these phenomena are causally related, studies have been made of the effects of forebrain ablations on the osmotically-induced release of oxytocin. In acute rabbit preparations the injection of 10 per cent NaCl into the carotid artery provided an osmotic stimulus. The milk-ejection technique was used to assess neurohypophysial activation. The hypertonic stimulus induced both a synchronous EEG firing of elements in the olfactory bulb and release of neurohypophysial hormone. However, after removal of the olfactory bulbs by blunt dissection and suction, the neurohypophysis could still be activated by the osmotic stimulus. In fact, only an hypothalamic island containing the supraoptic but not the paraventricular nuclei was necessary. The osmotic stimulus was no longer effective (with one questionable exception) after removal of the island, though the neurohypophysis still responded to direct electrical stimulation. Electrolytic lesions of the infundibular stalk blocked the reflex release of hormone. It was concluded that the osmotically-induced EEG response in the olfactory bulb is not essential for activation of the neurohypophysis and that osmoreceptors responsible for hormone release are located in the anterobasal part of the hypothalamus.