The spinal cord expression of neuronal and inducible nitric oxide synthases and their contribution in the maintenance of neuropathic pain in mice
Hervera Abad, Arnau (Universitat Autònoma de Barcelona. Institut de Neurociències)
Negrete, Roger (Universitat Autònoma de Barcelona. Institut de Neurociències)
Leánez, Sergi (Universitat Autònoma de Barcelona. Institut de Neurociències)
Martín-Campos, Jesús Martín (Institut d'Investigació Biomèdica Sant Pau)
Pol, Olga (Universitat Autònoma de Barcelona. Institut de Neurociències)

Fecha:	2010
Resumen:	Background: Nitric oxide generated by neuronal (NOS1), inducible (NOS2) or endothelial (NOS3) nitric oxide synthases contributes to pain processing, but the exact role of NOS1 and NOS2 in the maintenance of chronic peripheral neuropathic pain as well as the possible compensatory changes in their expression in the spinal cord of wild type (WT) and NOS knockout (KO) mice at 21 days after total sciatic nerve ligation remains unknown. Methodology/Principal Findings: The mechanical and thermal allodynia as well as thermal hyperalgesia induced by sciatic nerve injury was evaluated in WT, NOS1-KO and NOS2-KO mice from 1 to 21 days after surgery. The mRNA and protein levels of NOS1, NOS2 and NOS3 in the spinal cord of WT and KO mice, at 21 days after surgery, were also assessed. Sciatic nerve injury led to a neuropathic syndrome in WT mice, in contrast to the abolished mechanical allodynia and thermal hyperalgesia as well as the decreased or suppressed thermal allodynia observed in NOS1-KO and NOS2-KO animals, respectively. Sciatic nerve injury also increases the spinal cord expression of NOS1 and NOS2 isoforms, but not of NOS3, in WT and NOS1-KO mice respectively. Moreover, the presence of NOS2 is required to increase the spinal cord expression of NOS1 whereas an increased NOS1 expression might avoid the up-regulation of NOS2 in the spinal cord of nerve injured WT mice. Conclusions/Significance: These data suggest that the increased spinal cord expression of NOS1, regulated by NOS2, might be responsible for the maintenance of chronic peripheral neuropathic pain in mice and propose these enzymes as interesting therapeutic targets for their treatment.
Ayudas:	Instituto de Salud Carlos III PS0900968
Nota:	Altres ajuts: Fundació La Marató de TV3 Barcelona Grant: 070810
Derechos:	Aquest document està subjecte a una llicència d'ús Creative Commons. Es permet la reproducció total o parcial, la distribució, la comunicació pública de l'obra i la creació d'obres derivades, fins i tot amb finalitats comercials, sempre i quan es reconegui l'autoria de l'obra original.
Lengua:	Anglès
Documento:	Article ; Versió publicada
Materia:	Dolor ; Rates (Animals de laboratori) ; Experiments ; Neuropathic pain
Publicado en:	PloS one, Vol. 5, Issue 12 (December 2010) , p. e14321, ISSN 1932-6203

DOI: 10.1371/journal.pone.0014321
PMID: 21179208

8 p, 314.2 KB

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