Peripheral injury induces a programmed but reversible transformation of gene expression in somatosensory neurons providing a mechanism to regulate sensory input during wound healing.
Globotriaosylcermide directly impacts neuronal integrity and ion channel function as potential mechanism underlying small fiber pathology in Fabry disease.
Chronic pain distorts intensity coding in the anterior cingulate cortex to give rise to generalized anatomically nonspecific enhancement in pain aversion.
The flow of somatosensory information through the spinal dorsal horn is regulated by synaptic inhibition, which acts upon excitatory and inhibitory interneurons, but the former are especially prone to disinhibition.
Delayed intramuscular gene therapy with neurotrophin-3 after corticospinal tract injury reduces spasticity and improves locomotion by treating underlying causes of spasticity.
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.
Keratinocytes are critical for normal innocuous and noxious touch through their mechanically evoked ATP release and subsequent signaling to P2X4 channels on sensory neurons.
Stimulation of the rate-limiting enzyme in the NAD salvage pathway protected against neurotoxicity and subsequent peripheral neuropathy associated with the widely utilized anticancer drug, paclitaxel.
