Changes in mRNA for CAPON and Dexras1 in adult rat following sciatic nerve transection

J Chem Neuroanat. 2008 Jan;35(1):85-93. doi: 10.1016/j.jchemneu.2007.07.004. Epub 2007 Jul 31.

Abstract

Peripheral nerve transection has been implicated to cause a production of neuronal nitric oxide synthase (nNOS), which may influence a range of post-axotomy processes necessary for neuronal survival and nerve regeneration. Carboxy-terminal post synaptic density protein/Drosophila disc large tumor suppressor/zonula occuldens-1 protein (PDZ) ligand of neuronal nitric oxide synthase (CAPON), as an adaptor, interacts with nNOS via the PDZ domain helping regulate nNOS activity at postsynaptic sites in neurons. And Dexras1, a small G protein mediating multiple signal transductions, has been reported to form a complex with CAPON and nNOS. A role for the physiologic linkage by CAPON of nNOS to Dexras1 has suggested that NO-mediated activation of Dexras1 is markedly enhanced by CAPON. We investigated the changes in mRNA for CAPON, Dexras1 and nNOS in the sciatic nerve, dorsal root ganglia and lumbar spinal cord of adult rat following sciatic axotomy by TaqMan quantitative real-time PCR and in situ hybridization combined with immunofluorescence. Signals of mRNA for CAPON and Dexras1 were initially expressed in these neural tissues mentioned, transiently increased at certain time periods after sciatic axotomy and finally recovered to the basal level. It was also found that nNOS mRNA underwent a similar change pattern during this process. These results suggest that CAPON as well as Dexras1 may be involved in the different pathological conditions including nerve regeneration, neuron loss or survival and even pain process, possibly via regulating the nNOS activity or through the downstream targets of Dexras1.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptor Proteins, Signal Transducing / genetics*
  • Animals
  • Axotomy
  • Cell Survival / genetics
  • Female
  • Ganglia, Spinal / metabolism
  • Ganglia, Spinal / pathology
  • Ganglia, Spinal / physiopathology
  • Gene Expression Regulation, Enzymologic / genetics
  • In Situ Hybridization
  • Macromolecular Substances / metabolism
  • Male
  • Nerve Regeneration / genetics
  • Nitric Oxide / biosynthesis*
  • Nitric Oxide Synthase Type I / metabolism*
  • Posterior Horn Cells / metabolism
  • Posterior Horn Cells / pathology
  • Posterior Horn Cells / physiopathology
  • RNA, Messenger / analysis
  • RNA, Messenger / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Reverse Transcriptase Polymerase Chain Reaction
  • Sciatic Neuropathy / genetics
  • Sciatic Neuropathy / metabolism*
  • Sciatic Neuropathy / physiopathology
  • Spinal Nerve Roots / metabolism
  • Spinal Nerve Roots / pathology
  • Wallerian Degeneration / genetics
  • Wallerian Degeneration / metabolism
  • Wallerian Degeneration / physiopathology
  • ras Proteins / genetics*

Substances

  • Adaptor Proteins, Signal Transducing
  • Macromolecular Substances
  • NOS1AP protein, rat
  • RNA, Messenger
  • Rasd1 protein, rat
  • Nitric Oxide
  • Nitric Oxide Synthase Type I
  • Rasd1 protein, mouse
  • ras Proteins