The body defends against reduced extracellular fluid volume both by activation of autonomic and endocrine reflexes and by mobilization of behavioral mechanisms. The behaviors that are required to correct an extracellular fluid deficit involve the ingestion of both water and sodium. It is reasonable to hypothesize that afferent neural input from both arterial and cardiopulmonary high pressure and volume receptors, and afferent humoral input in the form of ANG II, are important systemically-generated signals acting as afferent mediators of extracellular depletion-induced thirst and sodium appetite. Neural information from these signals has been shown to converge on forebrain structures located along the lamina terminalis where processing and integration of this input is likely to take place. This paper describes an analysis of the mechanisms of afferent signaling that accompanies a form of rapidly induced sodium appetite. Because volume and pressure-related input in concert with elevated activity of the renin-angiotensin system is likely to be important for generating this form of induced hypertonic sodium chloride and water intake, we have focused on the structures of the lamina terminalis, specifically the SFO, MnPO, and OVLT. Investigations that employ immunocytochemical methods for the detection of the early oncogene, c-fos, indicate that neurons in the lamina terminalis, as well as the SON and PVN, are activated by the composite of systemically derived signals necessary for producing thirst and sodium appetite. So far, there is no thorough understanding of how these visceral signals activate the neural substrates for these motivated behaviors. However, these studies, combining both functional and neuroanatomical approaches, provide a strategy for investigating the neurobiological basis of the behavioral and physiological control systems that maintain fluid balance and cardiovascular homeostasis. This paper describes an analysis of the mechanisms of afferent signaling that accompanies a form of rapidly induced sodium appetite. Because volume and pressure-related input, in concert with elevated activity of the renin-angiotensin system, is likely to be important for generating this form of induced hypertonic sodium chloride and water intake, we have focused on the structures of the lamina terminalis, specifically the SFO, MnPO, and OVLT. Investigations that employ immunocytochemical methods for the detection of the early oncogene, c-fos, indicate that neurons in the lamina terminalis, as well as the SON and PVN, are activated by the composite of systemically derived signals necessary for producing thirst and sodium appetite. So far, there is no thorough understanding of how these visceral sensory-related signals activate the neural substrates for these motivated behaviors.(ABSTRACT TRUNCATED AT 400 WORDS)