Serotonin neurons integrate GABA and dopamine inputs to regulate meal initiation.

Obesity is a growing global health epidemic with limited orally administered therapeutics. Serotonin (5-HT) is one neurotransmitter which remains an excellent target for new weight-loss therapies, but a gap remains in understanding the mechanisms involved in 5-HT produced in the dorsal Raphe nucleus (DRN) and its involvement in meal initiation. Using an optogenetic feeding paradigm, we showed that the 5-HT➔arcuate nucleus (ARH) circuit plays a role in meal initiation.

Pulmonary Sequestration Masquerading as Pulmonary Abscess.

Pulmonary sequestration is a rare congenital condition wherein a nonfunctional lung segment, arising separately from the true lung bud, develops within the chest cavity but lacks communication with the tracheobronchial tree or pulmonary arterial supply. While this condition is typically diagnosed in children, our case highlights its relevance in adults. We present a 37-year-old male who presented with shortness of breath and was initially diagnosed with a pulmonary abscess.

Identification of an ionic mechanism for ERα-mediated rapid excitation in neurons.

The major female ovarian hormone, 17β-estradiol (E), can alter neuronal excitability within milliseconds to regulate a variety of physiological processes. Estrogen receptor-α (ERα), classically known as a nuclear receptor, exists as a membrane-bound receptor to mediate this rapid action of E, but the ionic mechanisms remain unclear. Here, we show that a membrane channel protein, chloride intracellular channel protein-1 (Clic1), can physically interact with ERα with a preference to the membrane-bound ERα.

Distinct basal forebrain-originated neural circuits promote homoeostatic feeding and suppress hedonic feeding in male mice.

Feeding behaviour is influenced by two primary factors: homoeostatic needs driven by hunger and hedonic desires for pleasure even in the absence of hunger. While efficient homoeostatic feeding is vital for survival, excessive hedonic feeding can lead to adverse consequences such as obesity and metabolic dysregulations. However, the neurobiological mechanisms that orchestrate homoeostatic versus hedonic food consumption remain largely unknown.

Loss of transient receptor potential channel 5 causes obesity and postpartum depression.

Hypothalamic neural circuits regulate instinctive behaviors such as food seeking, the fight/flight response, socialization, and maternal care. Here, we identified microdeletions on chromosome Xq23 disrupting the brain-expressed transient receptor potential (TRP) channel 5 (TRPC5). This family of channels detects sensory stimuli and converts them into electrical signals interpretable by the brain.