Craving for alcohol in the rat: adjunctive behavior and the lateral hypothalamus.

A review of previous results and the new data in this report show clearly that the Falk model of adjunctive behavior is an adequate analogue of human alcoholism and can be applied to induce excessive ethanol consumption. New data on the consumption of sweet flavored ethanol solutions and, especially, sweet alone solutions during brief periods of ethanol withdrawal provide some significant insights concerning the possible physiological basis for cravings in humans. Because voluntary consumption of ethanol is the normal process by which alcoholism develops, a general set of environmental and other experimental conditions that produce behavioral excess; adjunctive behavior, electrical stimulation of the brain, and salt arousal of drinking are discussed in some detail. Neuronal circuits of the lateral hypothalamus are important because some of the cells are chemosensitive and monitor osmolality of the blood and initiate drinking in the normal regulation of body fluids. Alcohol in very small amounts has a direct effect on these cells that also project to lower spinal motor neurons and modulate the level of excitability in spinal reflexes and thereby reactivity to environmental stimulation. Taste and other sensory information from the mouth arrives in presynaptic endings on these same cells by a multitude of indirect multisynaptic pathways. A theoretical model is developed to explain how tactile and taste sensory information and what is initially a nonspecific general state of motor arousal interact together to produce an excessive consumption or craving for ethanol.