NADPH oxidase-4 maintains neuropathic pain after peripheral nerve injury.
J Neurosci
; 32(30): 10136-45, 2012 Jul 25.
Article
en En
| MEDLINE
| ID: mdl-22836249
ABSTRACT
Reactive oxygen species (ROS) contribute to sensitization of pain pathways during neuropathic pain, but little is known about the primary sources of ROS production and how ROS mediate pain sensitization. Here, we show that the NADPH oxidase isoform Nox4, a major ROS source in somatic cells, is expressed in a subset of nonpeptidergic nociceptors and myelinated dorsal root ganglia neurons. Mice lacking Nox4 demonstrated a substantially reduced late-phase neuropathic pain behavior after peripheral nerve injury. The loss of Nox4 markedly attenuated injury-induced ROS production and dysmyelination processes of peripheral nerves. Moreover, persisting neuropathic pain behavior was inhibited after tamoxifen-induced deletion of Nox4 in adult transgenic mice. Our results suggest that Nox4 essentially contributes to nociceptive processing in neuropathic pain states. Accordingly, inhibition of Nox4 may provide a novel therapeutic modality for the treatment of neuropathic pain.
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Nervio Ciático
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NADPH Oxidasas
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Traumatismos de los Nervios Periféricos
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Neuralgia
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Neuronas
Límite:
Animals
Idioma:
En
Revista:
J Neurosci
Año:
2012
Tipo del documento:
Article
País de afiliación:
Alemania