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KMID : 0363120080210010011
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Korean Journal of Pain
2008 Volume.21 No. 1 p.11 ~ p.17
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The Expression of the Ca＋＋ Channel α2δ Subunit and TRPM8 in the Dorsal Root Ganglion of Sympathetically Maintained Pain and Sympathetic Independent Pain Rat Models
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Han Dong-Woo
Kweon Tae-Dong
Lee Youn-Woo
Kim Yeon-A
Choi Jong-Bum
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Abstract
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Background: Peripheral nerve injury induces up-regulation of the calcium channel alpha2delta (α2δ) subunit
and TRPM8 in the dorsal root ganglion (DRG) which might contribute to allodynia development. We investigated
the expression of the α2δ subunit and TRPM8 in the DRG of sympathetically maintained pain (SMP) and
sympathetic independent pain (SIP) rat model.
Methods: For the SMP model, the L5 and L6 spinal nerves were ligated tightly distal to the DRG. For the
SIP model, the tibial and sural nerves were transected, while the common peroneal nerve was spared. After
a 7 day postoperative period, tactile and cold allodynia were assessed using von Frey filaments and acetone
drops, respectively. Expression of the α2δ subunit and TRPM8 in the L5 and L6 DRG were subsequently
examined by a Western blot.
Results: There were no significant differences between the two models for the thresholds of tactile and cold
allodynia. Expression of the α2δ subunit in the ipsilateral DRG to the injury was increased as determined on
a Western blot as compared to that in the contralateral or sham-operated DRG of the SMP model, but there
was no difference in expression seen with the use of the SIP model. There was no difference in the expression
of TRPM8 in the ipsilateral DRG to the injury and the contralateral or sham-operated DRG of either model.
Conclusions: Up-regulation of the α2δ subunit in injured DRG may play a role that contributes to tactile
allodynia development in SMP, but not TRPM8 to cold allodynia after peripheral nerve injury. (Korean J Pain
2008; 21: 11?17)
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KEYWORD
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α2δ subunit, dorsal root ganglion, SIP, SMP, TRPM8
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