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, 2013, 170910

Low Frequency Electroacupuncture Alleviated Spinal Nerve Ligation Induced Mechanical Allodynia by Inhibiting TRPV1 Upregulation in Ipsilateral Undamaged Dorsal Root Ganglia in Rats

Affiliations

Low Frequency Electroacupuncture Alleviated Spinal Nerve Ligation Induced Mechanical Allodynia by Inhibiting TRPV1 Upregulation in Ipsilateral Undamaged Dorsal Root Ganglia in Rats

Yong-Liang Jiang et al. Evid Based Complement Alternat Med.

Abstract

Neuropathic pain is an intractable problem in clinical practice. Accumulating evidence shows that electroacupuncture (EA) with low frequency can effectively relieve neuropathic pain. Transient receptor potential vanilloid type 1 (TRPV1) plays a key role in neuropathic pain. The study aimed to investigate whether neuropathic pain relieved by EA administration correlates with TRPV1 inhibition. Neuropathic pain was induced by right L5 spinal nerve ligation (SNL) in rats. 2 Hz EA stimulation was administered. SNL induced mechanical allodynia in ipsilateral hind paw. SNL caused a significant reduction of TRPV1 expression in ipsilateral L5 dorsal root ganglia (DRG), but a significant up-regulation in ipsilateral L4 and L6 DRGs. Calcitonin gene-related peptide (CGRP) change was consistent with that of TRPV1. EA alleviated mechanical allodynia, and inhibited TRPV1 and CGRP overexpressions in ipsilateral L4 and L6 DRGs. SNL did not decrease pain threshold of contralateral hind paw, and TRPV1 expression was not changed in contralateral L5 DRG. 0.001, 0.01 mg/kg TRPV1 agonist 6'-IRTX fully blocked EA analgesia in ipsilateral hind paw. 0.01 mg/kg 6'-IRTX also significantly decreased pain threshold of contralateral paw. These results indicated that inhibition of TRPV1 up-regulation in ipsilateral adjacent undamaged DRGs contributed to low frequency EA analgesia for mechanical allodynia induced by spinal nerve ligation.

Figures

Figure 1
Figure 1
Effects of 2 Hz EA on bilateral paw withdrawal thresholds of rats subject to right L5 spinal nerve ligation. Data are presented as mean ± SEM, n = 8 per group. ***P < 0.001, SNL group versus normal group; # P < 0.05, ## P < 0.01, SNL + EA group versus SNL group.
Figure 2
Figure 2
Immunofluorescence of TRPV1 expressions in ipsilateral L5, L4, and L6 and contralateral L5 DRGs in normal, SNL, and SNL + EA groups. TRPV1-IR is mainly seen in small-to-medium DRG neurons (20–50 μm). Scale bar, 50 μm for all.
Figure 3
Figure 3
Western blotting analysis of TRPV1 levels in ipsilateral L5, L4, and L6 and contralateral L5 DRGs in normal, SNL, and SNL + EA groups. Results were expressed as relative fold changes as compared to normal group after normalization to β-actin. Data are presented as mean ± SEM of three independent experiments. *P < 0.05, **P < 0.01, SNL group or SNL + EA group versus normal group; ## P < 0.01, ### P < 0.001, SNL + EA group versus SNL group.
Figure 4
Figure 4
Western blotting analysis of CGRP levels in ipsilateral L5, L4, and L6 DRGs in normal, SNL, and SNL + EA groups. Results were expressed as relative fold changes as compared to normal group after normalization to β-actin. Data are presented as mean ± SEM of three independent experiments. *P < 0.05, **P < 0.01, SNL group or SNL + EA group versus normal group; ## P < 0.01, ### P < 0.001, SNL + EA group versus SNL group.
Figure 5
Figure 5
TRPV1 agonist 6′-IRTX blocked the antiallodynic effect of 2 Hz EA. 6′-IRTX was intraperitoneally injected 10 min before 2 Hz EA treatment on day 15. Data are presented as mean ± SEM, n = 8 per group. *P < 0.05, ***P < 0.001, SNL + EA + 0.001 mg/kg 6′-IRTX group or SNL + EA + 0.01 mg/kg 6′-IRTX group versus SNL + EA + vehicle group; # P < 0.05, SNL + EA + 0.01 mg/kg 6′-IRTX group versus SNL + EA + 0.001 mg/kg 6′-IRTX group.

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