The objective of this study is to investigate the neural and neuroendocrine mechanisms triggered by increases in plasma osmolality. We will test the hypothesis that stimuli signalling reductions in intracellular volume to bring about body fluid homeostasis originate primarily in areas within the anteroventral third ventricle (AV3V) area and secondarily in areas surrounding the supraoptic nucleus. To accomplish these goals, we will employ the quantitative autoradiographic (14C)deoxyglucose technique.
The specific aims of this study are: 1. To measure water intake and glucose utilization in the brain and hypothalamo-neurohypophysial system during intracarotid or intracerebroventricular infusion of hypertonic saline. This study will allow us to: 1) identify the body fluid homeostatic neural pathways involved in the osmoreceptor reflex; and 2) examine whether infusion of hypertonic saline by different routes activate the same neural substrates to bring about body fluid homeostasis. 2. To compare the effects of lesion of the AV3V area with that of sham-operated animals on glucose utilization in the pathways activated by different concentrations of intracarotid or intracerebroventricular infusions of hypertonic saline and relate them with the animal's water drinking behavior. This study will allow us to identify whether the afferent limb of the osmoreceptor reflex originates or crosses in the AV3V area and whether other mechanisms outside the AV3V area can be activated by a higher degree of plasma or cerebrospinal fluid osmolality. 3. To compare the effects of intravenous administration of hexamethonium, a nicotinic blocker agent, and phenoxybenzamine, an alpha-adrenergic blocker, on the basal activity and on the hyperosmotic-stimulated activity of the hypothalamo- neurohypophysial system and relate these findings with the animals, water drinking behavior. This study will allow us to understand how the cholinergic and adrenergic mechanisms are functionally related in the osmoreceptor reflex pathway.
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