Genetic subtype differences in neural circuitry of food motivation in Prader-Willi syndrome. Neural mechanisms underlying hyperphagia in Prader–Willi syndrome. Neural mechanisms underlying food motivation in children and adolescents. Behavioral differences among subjects with Prader–Willi syndrome and type I or type II deletion and maternal disomy. Ventral tegmental dopamine neurons participate in reward identity predictions. GLP-1 neurons in the nucleus of the solitary tract project directly to the ventral tegmental area and nucleus accumbens to control for food intake. Amphetamine paradoxically augments exocytotic dopamine release and phasic dopamine signals. The cerebellum in feeding control: possible function and mechanism. Cerebellar afferents from the nucleus of the solitary tract. Natural and drug rewards engage distinct pathways that converge on coordinated hypothalamic and reward circuits. Neurons for hunger and thirst transmit a negative-valence teaching signal. Sensory detection of food rapidly modulates arcuate feeding circuits. Neural representations of hunger and satiety in Prader–Willi syndrome. Is dopamine a physiologically relevant mediator of feeding behavior? Trends Neurosci. Nucleus accumbens dopamine and the regulation of effort in food-seeking behavior: implications for studies of natural motivation, psychiatry, and drug abuse. Cerebellar modulation of the reward circuitry and social behavior. Parallel, redundant circuit organization for homeostatic control of feeding behavior. Cerebellar nuclei evolved by repeatedly duplicating a conserved cell-type set. Synergistic interaction between leptin and cholecystokinin to reduce short-term food intake in lean mice. Importance of reward and prefrontal circuitry in hunger and satiety: Prader-Willi syndrome vs simple obesity. Prader–Willi syndrome: a review of clinical, genetic, and endocrine findings. Neural control of energy balance: translating circuits to therapies. The neurobiology of food intake in an obesogenic environment. Overlapping brain circuits for homeostatic and hedonic feeding. A nonadaptive scenario explaining the genetic predisposition to obesity: the “predation release” hypothesis. Our study defines a conserved satiation centre that may represent a novel therapeutic target for the management of excessive eating, and underscores the utility of a ‘bedside-to-bench’ approach for the identification of neural circuits that influence behaviour.īerthoud, H. We found that aDCN activity terminates food intake by increasing striatal dopamine levels and attenuating the phasic dopamine response to subsequent food consumption. Selective activation of aDCN neurons substantially decreased food intake by reducing meal size without compensatory changes to metabolic rate. Transcriptomic analyses in mice revealed molecularly and topographically -distinct neurons in the anterior deep cerebellar nuclei (aDCN) that are activated by feeding or nutrient infusion in the gut. Unbiased, task-based functional magnetic resonance imaging revealed marked differences in cerebellar responses to food in people with a genetic disorder characterized by insatiable appetite. Here we used a reverse-translational approach to identify and anatomically, molecularly and functionally characterize a neural ensemble that promotes satiation. However, our inability to control the increasing prevalence of obesity highlights a need to look beyond canonical feeding pathways to broaden our understanding of body weight control 1, 2, 3. The brain is the seat of body weight homeostasis.
0 kommentar(er)
