Hsiao, I.-H.; Yen, C.-M.; Hsu, H.-C.; Liao, H.-Y.; Lin, Y.-W. Chemogenetics Modulation of Electroacupuncture Analgesia in Mice Spared Nerve Injury-Induced Neuropathic Pain through TRPV1 Signaling Pathway. Int. J. Mol. Sci.2024, 25, 1771.
Hsiao, I.-H.; Yen, C.-M.; Hsu, H.-C.; Liao, H.-Y.; Lin, Y.-W. Chemogenetics Modulation of Electroacupuncture Analgesia in Mice Spared Nerve Injury-Induced Neuropathic Pain through TRPV1 Signaling Pathway. Int. J. Mol. Sci. 2024, 25, 1771.
Hsiao, I.-H.; Yen, C.-M.; Hsu, H.-C.; Liao, H.-Y.; Lin, Y.-W. Chemogenetics Modulation of Electroacupuncture Analgesia in Mice Spared Nerve Injury-Induced Neuropathic Pain through TRPV1 Signaling Pathway. Int. J. Mol. Sci.2024, 25, 1771.
Hsiao, I.-H.; Yen, C.-M.; Hsu, H.-C.; Liao, H.-Y.; Lin, Y.-W. Chemogenetics Modulation of Electroacupuncture Analgesia in Mice Spared Nerve Injury-Induced Neuropathic Pain through TRPV1 Signaling Pathway. Int. J. Mol. Sci. 2024, 25, 1771.
Abstract
Neuropathic pain is initiated by a malfunction of the somatosensory cortex system. Acupuncture had been shown to have therapeutic effects for neuropathic pain, although with uncertain mechanisms. We used electroacupuncture (EA) to treat mice spared nerve injury (SNI) model and explore the underlying molecular mechanisms through novel chemogenetic techniques. Both me-chanical and thermal pain were found in SNI mice till four weeks (mechanical: 3.23 ± 0.29 g; thermal: 4.9 ± 0.14 s). Hyperalgesia was attenuated by 2 Hz EA (mechanical: 4.05 ± 0.19 g; ther-mal: 6.22 ± 0.26 s) but not with sham EA (mechanical: 3.13 ± 0.23 g; thermal: 4.58 ± 0.37 s), sug-gesting EA’s specificity. In addition, animals with transient receptor potential V1 (Trpv1) deletion showed no significant induction of neuropathic pain (mechanical: 4.43 ± 0.26 g; thermal: 6.24 ± 0.09 s). Moreover, we found increased levels of inflammatory factors such as interleukin-1 beta (IL1-β), IL-3, IL-6, IL-12, IL-17, tumor necrosis factor alpha, and interferon gamma after SNI modeling, which decreased in EA and Trpv1-/- group rather than sham group. Western blot and immunofluorescence analysis showed similar tendency in the dorsal root ganglion, spinal cord dorsal horn, somatosensory cortex (SSC), and anterior cingulate cortex (ACC). In addition, a novel chemogenetics method was used to precisely inhibit SSC to ACC activity showed an analgesic effect through TRPV1 pathway. In summary, our findings indicate a novel mechanism underlying neuropathic pain as beneficial targets for neuropathic pain.
Biology and Life Sciences, Neuroscience and Neurology
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