Journal
JOURNAL OF NEUROSCIENCE
Volume 26, Issue 46, Pages 11974-11986Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.3188-06.2006
Keywords
p75 neurotrophin receptor; nerve growth factor; p38 mitogen-activated protein kinase; transient receptor potential channels; primary afferent neurons; neuropathic pain
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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.
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