Biology subjects

Azevedo, E.

Publications and source records attributed to Azevedo, E..

2 recordsLinked to original sources

bioRxiv2019

Lateral septum neurotensin neurons link stress and anorexia

Stress and anxiety are precipitating factors for eating disorders, but the neural basis linking stress to alterations in feeding is not well understood. Here we describe a novel population of stress-responsive neurons in the lateral septum (LS) of mice that express neurotensin (LSNTS) in a sexually dimorphic, estrous cycle-dependent manner. We used in vivo imaging to show that LSNTS neurons are activated by stressful experiences when flight is a viable option, but not by a stressful experience associated with freezing or immobility. LSNTS activation leads to a decrease of food intake and body weight in mice, without altering locomotion or other behaviors associated with anxiety. Molecular profiling of LSNTS neurons showed that these neurons co-express Glp1r (glucagon-like peptide 1 receptor), and both pharmacologic and genetic manipulations of Glp1r signaling in the LS recapitulates the behavioral effects of LSNTS activation. Finally, we mapped the outputs of LSNTS neurons and show that activation of LSNTS nerve terminals in the lateral hypothalamus (LH), a well-established feeding center, also decrease food intake. Taken together, these results show that LSNTS neurons link stress and anorexia via effects on hypothalamic pathways regulating food intake.

neuroscience↗

bioRxiv2019

A molecularly defined insular cortex --> central amygdala circuit mediates conditioned overconsumption of food.

Feeding is a complex motivated behavior that is controlled not just by metabolic and homeostatic factors, but also by environmental factors such as emotion and the hedonic nature of the food itself. Yet, little is known about how brain regions involved in cognition and emotion might contribute to overeating, and therefore, obesity. We used a recently developed behavioral task in which learned contextual cues induce feeding even in sated mice to investigate the underlying neural mechanisms. Using viral tracing, molecular profiling and chemo/optogenetic techniques, we discovered that an insular cortex projection to the central amygdala is required for conditioned overconsumption but not homeostatic feeding. The projection neurons express nitric oxide synthase-1 and activation of this population suppresses satiety signals in the central amygdala. The data thus indicate that the insular cortex provides top down control of homeostatic circuits to promote overconsumption in response to learned cues.\n\nOne Sentence SummaryNitric oxide synthase-1 neurons in the insular cortex promote overconsumption by projecting to the central amygdala to suppress a homeostatic satiety signal.

neuroscience↗