Early postembryonic bodily movement sends neural feedback through dorsal root ganglia to the forebrain in order to regulate the rate of neurogenesis and subsequent brain growth.

Molecular analysis paints a detailed picture of the distinctiveness and complexities of peripheral somatosensory neurons.

Human sensory neurons may not only bridge a critical gap between drug discovery and clinical trials, but force a re-evaluation of basic assumptions about the mechanisms controlling primary afferent excitability.

In the injured sciatic nerve, blood-derived monocytes and macrophages eat dying leukocytes, thereby contributing to nerve debridement and inflammation resolution, and this correlates with neuronal regeneration.

A cationic molecule derived from an uncharged Cav2.2 calcium channel inhibitor powerfully inhibits both sodium and calcium channels with extracellular application and inhibits both pain and neurogenic inflammation.

Electrophysiological experiments, Ca²⁺ imaging, and behavioral studies in mice identify the TRPM3 ion channel as a novel target of G-protein βγ subunits.

In Drosophila, the loss of Frataxin causes iron accumulation in the nervous system, which in turn enhances sphingolipid synthesis and activation of PDK1 and Mef2, which leads to neurodegeneration.

Channel activity is a novel regulatory mechanism for channel mobility in the plasma membrane.

Globotriaosylcermide directly impacts neuronal integrity and ion channel function as potential mechanism underlying small fiber pathology in Fabry disease.

Bile acid and it's receptor MRGPRX4, but not TGR5, is one of the ligand-receptor pairs for chronic itch in patients with liver diseases.