Meeting Abstract
Neuropeptide Y (NPY) is a conserved hypothalamic regulator of food intake in vertebrates, where it promotes the hunger response to encourage foraging. In addition, NPY has a complex interaction with components of the stress response both within the brain and on peripheral tissues. During a stress response, a hormonal cascade initiating in the hypothalamus, and acting through the anterior pituitary gland, eventually results in the release of glucocorticoid steroid hormones, such as corticosterone (CORT) into general circulation. Recent studies suggest that NPY can interact directly with the adrenal gland to facilitate CORT secretion. This interaction has been explored in mammals, where NPY receptors have been found on adrenal tissue, yet the general role of NPY in reptiles remains understudied. This raises the question of whether NPY can stimulate a stress response and whether a functioning stress response is required for NPY to exert its effects on food intake. Using the invasive brown anole (Anolis sagrei) we tested the hypothesis that NPY promotes both food intake and also CORT release. First, to test whether NPY can activate the stress response, we injected male anole lizards with either: 1) saline; 2) NPY; 3) dexamethasone, a glucocorticoid agonist which suppresses CORT release; or 4) both NPY and DEX. One hour after injection a blood sample was collected to measure plasma CORT concentrations. Second, we tested how the above treatments influenced food intake in captive anoles, by measuring the number of mealworms consumed post-injection. Injection with DEX did not increase food intake above control animals, suggesting CORT release does not itself alter feeding. Current studies are continuing to elucidate the dynamic and complex relationship between NPY, food intake, and stress.
