1991 Volume 31 Issue 3 Pages 245-251
The central nervous system is important in coordinating behavioral and autonomic control of homeostasis in response to outer and inner environmental changes. Multiplex neuronal networks of efferent and afferent autonomic nerves, plus various neuronal structures contribute to integration of information to control feeding behavior as well as visceral functions. Chemosensitive neurons in the lateral hypothalamic area (LHA) that receive and respond to humoral information, such as blood-borne chemicals and hormones, have been identified in this area. The information received here by the chemosensitive neurons themselves, or through afferent neuronal connection from the brain stem or viscera is further integrated by communication between the hypothalamus and the association cortices. The LHA also regulates autonomic nerve projections to visceral organs such as the liver, pancress and gastrointestinal tract through the efferent path to the autonomic preganglionic neurons in the brain stem and the spinal cord. Intracerebroventricular administration of 2-deoxy-D-glucose (2-DG) induced feeding behavior, hyperglycemia, and excitation and inhibition of LHA neuronal activity which indicates involvement of LHA chemosensitive neurons in the control of feeding behavior. Direct application of 2-DG into the LHA increased adrenal sympathetic nerve activity and decreased sympathetic nerve activity to the brown adipose tissue (BAT). This indicates that glucoprivation induced by 2-DG affects LHA neuronal activity, and some of the signals received by chemosensitive neurons are reflected in the control of behavior, while others are projected to the autonomic nervous system. Excitatory effects on adrenal nerves promote catecholamine secretion and hyperglycemia. Inhibitory effects on BAT sympathetic nerves suppress thermogenesis and energy expenditure in this tissue. All of these responses are considered to be necesary for the maintenance of the homeostasis in response to a challenge of the central nervous system. From this view point, disturbance of feeding behavior in obese patients is considered to be a result of abnormality in the transduction of information that simultaneously controls behavior and visceral functions. These patients have unbalance and dissociation of communication between the association cortices, the hypothalamus and peripheral metabolism. Consequently, higher functions such as memory and motivation in cortical neurons, and external information received by them strongly effect their feeding behavior. Behavioral disorder in obese patients can impair peripheral metabolism, and the resultant incorrect humoral information can further disturb behavioral control. One of the most important factors in the treatment of obesity is escape from this vicious cycle of information transduction. To accomplish that, it is necessary to input appropriate information produced by sensory signals into patients themselves. Their neuronal systems must be conditioned to detect the difference between correct and incorrect information, and reflect this ability in behavioral control. Finally, the recovery of physiological control is expected as an object of treatment.
