RT Journal Article
SR Electronic
T1 Suppression of the p75 Neurotrophin Receptor in Uninjured Sensory Neurons Reduces Neuropathic Pain after Nerve Injury
JF The Journal of Neuroscience
JO J. Neurosci.
FD Society for Neuroscience
SP 11974
OP 11986
DO 10.1523/JNEUROSCI.3188-06.2006
VO 26
IS 46
A1 Obata, Koichi
A1 Katsura, Hirokazu
A1 Sakurai, Jun
A1 Kobayashi, Kimiko
A1 Yamanaka, Hiroki
A1 Dai, Yi
A1 Fukuoka, Tetsuo
A1 Noguchi, Koichi
YR 2006
UL http://www.jneurosci.org/content/26/46/11974.abstract
AB The p75 neurotrophin receptor (p75NTR) has been implicated in diverse neuronal responses, including survival, cell death, myelination, and inhibition of regeneration. However, the role of p75NTR in neuropathic pain, for which there is currently no effective therapy, has not been explored. Here, we report that the pharmacological blockade of p75NTR in primary sensory neurons reversed neuropathic pain after nerve injury. Nerve injury increased the expression and axonal transport of p75NTR and phosphorylation of TrkA in the uninjured primary afferents. Functional inhibition of p75NTR suppressed injury-induced neuropathic pain and decreased the phosphorylation of TrkA and p38 mitogen-activated protein kinase, and the induction of transient receptor potential channels in dorsal root ganglion (DRG) neurons. Our results show that p75NTR induced in undamaged DRG neurons facilitates TrkA signaling and contributes to heat and cold hyperalgesia.