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. Coupled with in vitro mutagenesis, reverse genetics can be applied widely to accelerate progress in understanding the influenza virus life cycle, the generation of customized vaccine seed strains, development of live-attenuated vaccines, and the use of influenza virus as vaccine and gene delivery vectors.The brain is the seat of body weight homeostasis. Although continual improvement in reverse genetics system is being made in different laboratories for the efficient rescue of the influenza virus, the basic concept of synthesizing viral RNA using RNA polymerase I remains the same. Since its development in 1999, plasmid-based reverse genetics has been effectively applied to numerous aspects of influenza studies which include revolutionizing the production of seasonal and pandemic influenza vaccine seed strains. Reverse genetics is the creation of a virus from a full-length cDNA copy of the viral genome, referred to as an “infectious clone,” and is one of the most powerful genetic tools in modern virology.