MRGPRD and MRGRPX1 are co-expressed in primate DRG neurons, but β-alanine and BAM8-22, preferentially activate CMH-subclasses, and co-activating different cutaneous nociceptors by pruritogens does not change itch sensation to pain.

Sensory nerve fiber ending ensheathment and connexin 43 contacts by keratinocytes at the neuro-cutaneous unit can be visualized and quantified at super-resolution in human skin.

A system to generate ‘remote touch’ in freely behaving mice can be utilized to map behavior caused by precise somatosensory inputs.

In reporter mice, subtypes of peripheral neurons show different regenerative capabilities after nerve injury and activate common pathways but also specific ones, indicating a different intrinsic growth response among them.

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

Inflammatory pain, previously thought to result from increased activity in "pain" neurons, may in fact be due to wholesale changes in afferent output that includes increased and decreased activity that the brain interprets as pain.

The expression and function of the cation channel TRPM3 is strongly increased in sensory neurons innervating inflamed tissue, likely contributing to inflammatory hyperalgesia and persistent pain.

Keratinocytes are critical for normal innocuous and noxious touch through their mechanically evoked ATP release and subsequent signaling to P2X4 channels on sensory neurons.

Greater connectivity of the descending pain modulatory system network in the infant brain is associated with lower pain-related brain activity.

Single-nociceptor tracing reveals a novel somatotopic organization for the mammalian pain system, and physiological recordings and peripheral optogenetic behavior assays suggest that it is a possible mechanism underlying region-specific pain sensation.