The extrinsic cue NGF and the intrinsic signal Islet1 converge at the level of the Runx1/CBFβ transcription factor complex formation to promote differentiation of a major nociceptor subtype.
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.
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.
The mTOR downstream effector eukaryotic initiation factor 4E-binding protein 1 (4E-BP1) regulates mechanical nociception via translational control of synaptic transmission in the spinal cord.
A class of interneuron is identified that promotes escape behavior downstream of nociceptor inputs via connections to nociceptive integrator and premotor networks.
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.
Drosophila polymodal nociceptors use precipitous fluctuation of the firing rate, which depends on Ca2+ influx, as a key signal encoding a heat sensation and evoking the robust heat avoidance behavior.
An interdisciplinary approach uncovers a new antinociceptive molecular mechanism and shows that the adhesion GPCR CIRL adjusts the sensation of gentle touch and noxious mechanical insult in opposite directions.
A small population of lateral hypothalamic neurons detects pain and can be activated to suppress pain-related behavioral adaptations and the unpleasantness associated with pain in mice.
Cell-specific alternative splicing of the synaptic calcium channel gene Cacna1b is controlled by exon hypomethylation and CTCF binding and is disrupted following nerve injury.
