Understanding the neural control of ingestive behaviors: helping to separate cause from effect with...

Eating and drinking are motivated behaviors that are made up of coordinated sets of neuroendocrine, autonomic, and behavioral motor events. Although the spinal cord, hindbrain, and hypothalamus contain the motor neurons and circuitry sufficient to maintain the reflex parts of these motor events, inputs from the telencephalon are required to furnish the behavioral components with a motivated (goal-directed) character. Each of these motor events derives from the complex interaction of a variety of sensory inputs with groups of neural networks whose components are distributed throughout the brain and collectively support motor expression and coordination. At a first approximation based on a variety of data, these networks can be divided into three groups: networks that stimulate, those that inhibit, and those that disinhibit motor functions. A fourth contributor is the circadian timing signal that originates in the hypothalamic suprachiasmatic nucleus and provides the temporal anchor for the expression of all behaviors. This article discusses the nature of these networks using neuroanatomical (tract-tracing and neuropeptide in situ hybridization), endocrine, and behavioral evidence from a variety of experimental models. A persistent problem when studying the control of food intake from a neural systems perspective has been the difficulty in separating those neuronal changes that result in hunger from those that are as a consequence of eating. To address this problem, dehydration-associated anorexia is presented as a particularly useful experimental model because it can be used to distinguish between neural mechanisms underlying anorexia and those changes that occur as a consequence of anorexia. The article concludes by highlighting the potential role of neuropeptidergic action in the operation of these networks, using forebrain neuropeptidergic innervation of the parabrachial nucleus as an example.