Chronic pain distorts intensity coding in the anterior cingulate cortex to give rise to generalized anatomically nonspecific enhancement in pain aversion.
Globotriaosylcermide directly impacts neuronal integrity and ion channel function as potential mechanism underlying small fiber pathology in Fabry disease.
Peripheral injury induces a programmed but reversible transformation of gene expression in somatosensory neurons providing a mechanism to regulate sensory input during wound healing.
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.
A new spinal somatosensory preparation is described which enables fine control of sensory input and the ability to manipulate spinal interneurons while recording from spinal projection neurons.
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.
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.
