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Fasting-activated hypothalamic AgRP-expressing neurons trigger fasting-induced hypothalamic–pituitary–adrenal axis activation through projections to the paraventricular hypothalamus, where they activate CRH neurons by presynaptically inhibiting the terminals of tonically active GABAergic afferents from the bed nucleus of the stria terminalis.

Release of hunger-promoting and satiety-promoting neuropeptides drives opposing changes in the second messenger cAMP in awake mouse paraventricular hypothalamic MC4R neurons, thereby regulating synaptic plasticity and the transition to satiety with each bite of food.

Melanocortin 4 receptors (MC4Rs) are critical to the promotion of homeostatic satiety. The authors established paraventricular hypothalamus (PVH) MC4R-expressing neurons as a functional target for orexigenic arcuate nucleus agouti-related peptide–expressing neurons and identify an explicit PVH MC4R-expressing neuron to lateral parabrachial nucleus satiety-promoting circuit, the activation of which encodes positive valence in calorically depleted mice.

In response to food cues, a hypothalamic circuit in the mouse brain transiently inhibits neurons expressing agouti-related peptide, and this promotes learning of cue-initiated food-seeking tasks.

AgRP neurons of the arcuate nucleus of the hypothalamus promote homeostatic feeding yet are rapidly suppressed by food-related sensory cues. The authors identify a population of inhibitory DMH-LepR neurons that relays real-time information about the nature and availability of food to dynamically modulate ARC-AgRP neuron activity and feeding behavior.

Anatomical lesions of the preoptic area (POA) can cause sleep loss while electrical, chemical, or thermal stimulation of POA can induce sleep. To better understand the exact neural function of the POA, this study shows that galanin and GABA+ inhibitory neurons in the ventrolateral POA that project to the wake-promoting tuberomammillary nucleus promote sleep in a stimulation frequency dependent manner.

A combination of microprism-based cellular imaging to monitor insular cortex visual cue responses in behaving mice across hunger states with circuit mapping and manipulations reveals a neural basis for state-specific biased processing of motivationally relevant cues.

Hunger-promoting AgRP neurons and satiety-promoting POMC neurons in the arcuate nucleus mediate homeostatic regulation of hunger. Yet a rapidly acting satiety component analogous to rapidly hunger-promoting AgRP neurons has been missing. The authors identify this missing satiety signal and show that it is carried by a novel subset of arcuate glutamatergic neurons.

The AgRP-expressing neurons in the arcuate nucleus drive food-seeking behaviours during caloric restriction; a mouse study of monosynaptic retrograde rabies spread and optogenetic circuit mapping reveals that these neurons are activated by input from hypothalamic paraventricular nucleus cells and their activation or inhibition can modulate feeding behaviour.