PMID- 19524556
OWN - NLM
STAT- MEDLINE
DCOM- 20091215
LR  - 20121115
IS  - 1872-6240 (Electronic)
IS  - 0006-8993 (Linking)
VI  - 1285
DP  - 2009 Aug 18
TI  - Autotomy behavior correlates with the DRG and spinal expression of sodium 
      channels in inbred mouse strains.
PG  - 1-13
LID - 10.1016/j.brainres.2009.06.012 [doi]
AB  - Patients who have suffered nerve injury show profound inter-individual 
      variability in neuropathic pain even when the precipitating injury is nearly 
      identical. Variability in pain behavior is also observed across inbred strains of 
      mice where it has been attributed to genetic polymorphisms. Identification of 
      cellular correlates of pain variability across strains can advance the 
      understanding of underlying pain mechanisms. Voltage-gated sodium channels 
      (VGSCs) play a major role in the generation and propagation of action potentials 
      in the primary afferents and are therefore of obvious importance for pain 
      phenotype. Here, we examined the mRNA expression levels of the VGSC 
      alpha-subunits Na(v)1.3, Na(v)1.5, Na(v)1.6, and Na(v)1.7, as well as the 
      auxiliary VGSC-related molecule, Contactin. Dorsal root ganglia (DRG) and spinal 
      cords from 5 inbred mouse strains with contrasting pain phenotype (AKR/J, 
      C3H/HeJ, C57BL/6J, C58/J and CBA/J) were analyzed 7 days following sciatic and 
      saphenous nerve transection. In the DRG, Na(v)1.6, Na(v)1.7 and Contactin were 
      abundantly expressed in control animals. Following nerve injury, the residual 
      mRNA levels of Na(v)1.6 (downregulated in two of the strains) correlated tightly 
      to the extent of autotomy behavior. A suggestive correlation was also seen for 
      the post-injury mRNA levels of Contactin (downregulated in all strains) with 
      autotomy. Thus, our results suggest a contribution by DRG Na(v)1.6, and possibly 
      Contactin to neuropathic pain in the neuroma model in mice.
FAU - Persson, Anna-Karin
AU  - Persson AK
AD  - Center for Oral Biology, Novum, Karolinska Institutet, Huddinge, Sweden. 
      Anna-Karin.M.Persson@ki.se
FAU - Thun, Jonas
AU  - Thun J
FAU - Xu, Xiao-Jun
AU  - Xu XJ
FAU - Wiesenfeld-Hallin, Zsuzsanna
AU  - Wiesenfeld-Hallin Z
FAU - Strom, Mikael
AU  - Strom M
FAU - Devor, Marshall
AU  - Devor M
FAU - Lidman, Olle
AU  - Lidman O
FAU - Fried, Kaj
AU  - Fried K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20090611
PL  - Netherlands
TA  - Brain Res
JT  - Brain research
JID - 0045503
RN  - 0 (Cell Adhesion Molecules, Neuronal)
RN  - 0 (Contactins)
RN  - 0 (NAV1.6 Voltage-Gated Sodium Channel)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Scn8a protein, mouse)
RN  - 0 (Sodium Channels)
SB  - IM
MH  - Animals
MH  - Cell Adhesion Molecules, Neuronal/genetics/metabolism
MH  - Contactins
MH  - Disease Models, Animal
MH  - Ganglia, Spinal/*metabolism/physiopathology
MH  - Gene Expression Regulation/genetics
MH  - Ion Channel Gating/genetics
MH  - Mice
MH  - Mice, Inbred C3H
MH  - Mice, Inbred C57BL
MH  - Mice, Inbred CBA
MH  - NAV1.6 Voltage-Gated Sodium Channel
MH  - Nerve Tissue Proteins/genetics/metabolism
MH  - Neuralgia/genetics/metabolism/physiopathology
MH  - Nociceptors/metabolism
MH  - Peripheral Nervous System Diseases/genetics/*metabolism/physiopathology
MH  - Phenotype
MH  - Posterior Horn Cells/metabolism
MH  - RNA, Messenger/metabolism
MH  - Sciatic Neuropathy/genetics/metabolism/physiopathology
MH  - Self Mutilation/genetics/*metabolism/physiopathology
MH  - Sensory Receptor Cells/*metabolism
MH  - Sodium Channels/genetics/*metabolism
MH  - Species Specificity
MH  - Spinal Cord/*metabolism/physiopathology
EDAT- 2009/06/16 09:00
MHDA- 2009/12/16 06:00
CRDT- 2009/06/16 09:00
PHST- 2008/11/26 00:00 [received]
PHST- 2009/05/20 00:00 [revised]
PHST- 2009/06/03 00:00 [accepted]
PHST- 2009/06/16 09:00 [entrez]
PHST- 2009/06/16 09:00 [pubmed]
PHST- 2009/12/16 06:00 [medline]
AID - S0006-8993(09)01167-6 [pii]
AID - 10.1016/j.brainres.2009.06.012 [doi]
PST - ppublish
SO  - Brain Res. 2009 Aug 18;1285:1-13. doi: 10.1016/j.brainres.2009.06.012. Epub 2009 
      Jun 11.