Avian telencephalon and body weight

Abstract

The neurological mechanisms associated with weight gain in animals have been extensively studied in mammals, but relatively little investigation has been carried out in birds. As in mammals, it has been shown that lesion of the ventromedial nucleus of the hypothalamus leads to hyperphagia and obesity in several species of birds. Likewise, bilateral lesions of the lateral hypothalamus result in aphagia and weight loss. Therefore, at the level of the hypothalamus, control of body weight appears to be controlled by similar neurological mechanisms in all homeothermic species via modulation of the sympathetic nervous system. Because of the role of the mammalian striatum in body weight regulation, body weight data from various manipulative studies in chickens were analyzed to see if these areas play a role in avian body weight regulation. In the first study, cycloheximide, glutamate, or saline was injected intracerebrally into 1-day-old chicks. In the second study, 3-day-old chicks received surgical ablation of the neocortex or kainic acid-induced lesions of the paleostriatum. Decreased body weight was noted in chicks that received injections of cycloheximide or glutamate, or kainic acid-induced lesions. The disruption in body weight in Experiment 1 might have been due to neurochemical pathology thought to occur in the paleostriatum. In the second experiment, lesions of the neostriatum or hyperstriatum, analogous to the neocortex in mammals, did not produce a difference in weight gain compared to controls. This preliminary work with kainic acid lesions in the chicken paleostriatum demonstrates a significant long-term decrease in body weight. As in mammals, the basal ganglia may have a role in body weight regulation.