Vargas SL, Watts AG (2013) Compensatory feeding after reversing dehydration-anorexia: Is it analogous to glucoprivic or food deprivation-induced feeding?. Neuroscience 2013 Abstracts 757.04. Society for Neuroscience, San Diego, CA.
Summary: We use dehydration (DE)-anorexia to identify the neural networks associated with feeding behavior. How these networks are organized and interact to control ingestive behavior in both the normal and anorexic states allows us to determine how they function in health and disease. DE-anorexia involves replacing drinking water with hypertonic saline (HS) for up to 5 days. This leads to cellular dehydration, and a reduction in food and body weight. Reversing DE-anorexia by removing HS and reinstating drinking water leads to a robust feeding episode. Here we used two experiments to determine whether this water-activated compensatory feeding is functionally related to 2-deoxyglucose (2DG)-activated (glucoprivic) or to food deprivation-induced feeding. First, we determined whether forebrain-projection catecholamine (CA) neurons in the hindbrain are required for water-activated compensatory feeding. These neurons project to the paraventricular nucleus of the hypothalamus (PVH) and are required for 2DG feeding. To do this we lesioned this pathway with the retrogradely-transported immunotoxin, anti-dopamine beta-hydroxylase (DBH) Saporin (DSAP). Anesthetized adult male Sprague-Dawley rats (300g) were injected into the PVH with either a control SAP (MIgSAP) or DSAP. Three weeks later animals were housed in BioDaq monitoring cages to record their feeding behavior. All animals were given HS for 5 days. They were then given drinking water back on the 5th day, and euthanized 75 minutes later. Lack of immunohistochemical staining (IHC) for DBH in the PVH confirmed complete lesions. DSAP lesions had no significant effect on the amount eaten or the latency to begin feeding. Forebrain-projecting CA neurons are therefore not required for water-activated compensatory feeding. Second, we compared the feeding behavior of DE-rats given back water to that of food-deprived rats given food. We also examined the neuronal activity in the hindbrain of these animals using Fos. Meal pattern analysis showed little difference between groups, once feeding was initiated. Dual IHC labeling for Fos and DBH showed no colocalization following drinking water and deficit induced feeding. This contrasts with 2DG stimulated feeding. Furthermore, we show that the Fos expression in particular parts of the nucleus of the solitary tract and the parabrachial nucleus is consistent their roles in projecting visceral and gustatory information to the hypothalamus to coordinate feeding. Thus water-activated compensatory feeding engages mechanisms similar to those used during food deprivation-induced feeding rather than glucoprivic feeding.
Related Products: Anti-DBH-SAP (Cat. #IT-03)