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We have used the anorexia shown by rats given hypertonic saline to drink to investigate central mechanisms that can inhibit feeding. Rats dehydrated in this manner for 3 or 5 days showed a severe attenuation of the compensatory feeding observed after an overnight fast compared with control euhydrated rats or rats whose food was restricted to match the intake of anorexic rats. Food intake after injections of 2-deoxy-d-glucose (2-DG) was also significantly decreased in dehydrated animals compared with that after a 2-DG injection given before dehydration. However, all the dehydrated animals demonstrated a robust eating response after water was returned whether they had received injection of 2-DG or vehicle. Despite a profound reduction in 2-DG-induced feeding, other glucoregulatory responses to 2-DG remained intact in dehydrated animals. After 2-DG injection, corticosterone secretion and blood glucose were significantly elevated from preinjection values whether or not animals were dehydrated. Thus the mechanisms responsible for anorexia in dehydrated animals specifically target stimulatory feeding pathways but leave intact other counterregulatory glucometabolic motor events.

Many models have been proposed over the years to explain how motivated feeding behavior is controlled. One of the most compelling is based on the original concepts of Eliot Stellar whereby sets of interosensory and exterosensory inputs converge on a hypothalamic control network that can either stimulate or inhibit feeding. These inputs arise from information originating in the blood, the viscera, and the telencephalon. In this manner the relative strengths of the hypothalamic stimulatory and inhibitory networks at a particular time dictates how an animal feeds. Anorexia occurs when the balance within the networks consistently favors the restraint of feeding. This article discusses experimental evidence supporting a model whereby the increases in plasma osmolality that result from drinking hypertonic saline activate pathways projecting to neurons in the paraventricular nucleus of the hypothalamus (PVH) and lateral hypothalamic area (LHA). These neurons constitute the hypothalamic controller for ingestive behavior, and receive a set of afferent inputs from regions of the brain that process sensory information that is critical for different aspects of feeding. Important sets of inputs arise in the arcuate nucleus, the hindbrain, and in the telencephalon. Anorexia is generated in dehydrated animals by way of osmosensitive projections to the behavior control neurons in the PVH and LHA, rather than by actions on their afferent inputs.

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