Maintenance of appropriate body hydration is controlled by the brain and is essential to preserve extracellular fluid volume and tonicity. Upon dehydration, osmotic homeostasis is restored through coordinated responses such as thirst (to promote water intake) and vasopressin secretion (to promote water reabsorption by the kidneys). In addition to these responses, dehydration is known to suppress appetite. This dehydration-induced anorexia is a highly adaptive response to prevent the absorption of osmolytes from food. In this project, we aim to identify the stimuli and neural mechanisms driving this response.Dehydration is a combination of multiple stimuli: hyperosmolality (increased concentration of particles in the blood), hypernatremia (increased sodium concentration), and hypovolemia (reduced blood volume). We have found that food ingestion after an overnight fast acutely increases serum osmolality and sodium levels. Furthermore, we have found that all three dehydration stimuli – hyperosmolality, hypernatremia, and hypovolemia – suppress feeding, suggesting the involvement of multiple parallel brain circuits in this anorectic response.The organum vasculosum lamina terminalis (OVLT) is a circumventricular organ containing populations of neurons activated by hyperosmolality (via the osmosensitive ion channel ΔN-TRPV1), hypernatremia, and hypovolemia. Upon sensing disturbances to hydration balance, the OVLT triggers behavioural and physiological responses to maintain fluid homeostasis. We are currently investigating the involvement of specific OVLT neurons in the anorectic response to dehydration.