Specific circuits within the CNS are dedicated to the maintenance of homeostasis and an optimal cellular environment through regulation of autonomic function. Disease states such as fever, obesity, diabetes, hypertension, autonomic hyperreflexia and cardiac arrhythmia are associated with altered regulation of the sympathetic outflow to cardiovascular and non-cardiovascular tissues. The Morrison lab's research uses electrophysiological and anatomical approaches to understand the functional organization, rhythmicities, developmental influences and pharmacology of the CNS circuits that regulate the sympathetic outflows controlling variables critical for homeostasis such as body temperature, energy expenditure, blood glucose, blood pressure, cardiac output and plasma catecholamines.We are currently pursuing three main areas of investigation in the rapidly growing field of autonomic neuroscience. The first concerns the regulation of the sympathetic outflow to brown adipose tissue in the rat as a model system for gaining insight into the central circuits involved in regulating energy metabolism and body temperature. The results of these studies will be relevant to altered thermoregulation occurring during fever and to the increasing public health problem of obesity, which can be viewed as an imbalance between energy intake and metabolism. We are also studying the CNS regulation of catecholamine release from the adrenal medulla, an important component of a variety of stress responses including hypoglycemia, hemorrhage, and exercise. The third area of research involves the organization of the medullary pathways regulating sympathetic outflow to the cardiovascular system. These experiments have indicated a novel source of excitatory input to the neural circuits that generate sympathetic outflow, a result which will contribute to our understanding of the elevated blood pressure in models of hypertension such as the spontaneously hypertensive rat. By addressing basic questions in autonomic neuroscience, we seek to understand the altered regulation of sympathetic outputs characteristic of several disease states.