Hypothalamic circuits governing feeding and other motivated behaviors

Stress-induced negative emotion results in comfort eating. Here authors identify the enkephalinergic LH circuit and its interaction with stress hormone, corticosterone, as crucial players in the threat-induced emotional eating for palatable foods.

VTA glutamatergic neurons mediate innate defensive behaviors. Here, authors show that suppression of feeding induced by escape responses to threats is mediated by VTA glutamatergic neurons regulated by lateral hypothalamic glutamatergic neurons.

Food intake is determined by learned appetitive responses and physiological “appetition” signals after eating begins. Here, authors show melanin-concentrating hormone (MCH)-producing neurons integrate these processes to promote caloric intake.

Eating behviours consist of seeking and consummatory phases. Here, authors show that two distinct lateral hypothalamic leptin receptor neurons orchestrate seeking and consummatory phases of eating behaviour via hunger signal, Neuropeptide Y.

Using a murine diphtheria toxin ablation strategy, we have depleted afferent neurons expressing the Nav1.8 sodium channel and unravelled their functions in the control of energy homeostasis, highlighting their potential to address metabolic disorders.

In vivo recordings show that a subset of supramammillary neurons that project to the medial septum are wake-active, and projection-specific manipulations reveal that this hypothalamic-septal projection contributes to wakefulness modulation.

Infusing rats with an ultradian pattern of corticosterone, either in-phase or out-of-phase with lighting cues, has revealed how circadian misalignment induces dysregulated neuropeptide gene expression and disordered feeding behaviour.

Optogenetic or pharmacological modulation of hypocretin neurons impacts mouse impulsivity in a Go/No-Go task, suggesting that these neurons play a key role in integrating salient stimuli and guiding responses to various environmental cues.