Topic: feeding behavior

AIMS: The activation of CB1 receptor (CB1R) is reported to favor energy accumulation and promote resiliency against stress. The aim of this study is to elucidate whether CB1R expression in CaMKII+ neurons is sufficient to restore its role in the regulation of energy metabolism and contingent behaviors.METHODS: To this end, we applied a genetic strategy to reconstitute CB1R expression at endogenous levels in CaMKII+ neurons (CaMKII-CB1-RS).RESULTS: The rescue of CB1R expression in these neurons promotes feeding behavior causing fasting-induced hyperphagia, increased motivation and impulsivity t

Despite an overall increase in caloric needs, regular physical activity has been associated with improved appetite signaling. The neurobiological mechanisms underlying this sensitization remain unclear. We employed a voluntary wheel running protocol to investigate how physical activity affects gut-brain communication of vagal sensory neurons for the control of feeding behavior in mice. We find that physically active mice exhibit a significant decrease in food intake in response to the delivery of nutrients directly into the stomach, as compared to sedentary controls. Further, sensitivity to ch

Proopiomelanocortin neurons have been primarily described as controlling feeding behavior, but accumulating evidence also showed a crucial role of these neurons in the control of glucose homeostasis. For this, and in addition of being able to sense peripheral signals, POMC neurons receive direct upstream excitatory (glutamate) and inhibitory (GABA) inputs coming from a plethora of brain areas. Remarkably, EphrinBs (EphrinB1, B2, B3) proteins are well-known actor of glutamatergic synapse formation and plasticity. A study from our group showed that the modulation of EphrinB1 a during development

Hypothalamus is the center of energy metabolism and feeding behavior, and several hypothalamic neurotransmitters regulate energy homeostasis. Neurosecretory protein GL (NPGL) and neurosecretory protein GM (NPGM), were discovered as a novel neuropeptide from hypothalamus in 2014, induced obese phenotype owing to increased feeding behavior and lipogenesis in rats. However, the mechanisms of energy metabolism mediated by NPGL/NPGM system has not been totally elucidated. To investigate the loss of function of NPGL/NPGM system in mammals, we have established NPGL and NPGM double knockout mice (NPGL

It is well known that the state of hunger can modulate hormones and hypothalamic neural circuits to drive food-seeking behavior and consumption. While the olfactory sense is critical to foraging, the role of the olfactory cortex in regulating food learning and preference is unclear. The anterior piriform cortex (APC) is located one synapse downstream of the olfactory bulb and is an important olfactory structure for odor discrimination, perception, and memory. Here, we investigated whether acute fasting in mice can alter an odor-guided foraging behavior and how it can alter neurons and synapses