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Microglial deactivation by adeno‐associated virus expressing small‐hairpin GCH1 has protective effects against neuropathic pain development in a spinothalamic tract‐lesion model
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Microglial deactivation by adeno‐associated virus expressing small‐hairpin GCH1 has protective effects against neuropathic pain development in a spinothalamic tract‐lesion model
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Microglial deactivation by adeno‐associated virus expressing small‐hairpin GCH1 has protective effects against neuropathic pain development in a spinothalamic tract‐lesion model
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Journal Article
Microglial deactivation by adeno‐associated virus expressing small‐hairpin GCH1 has protective effects against neuropathic pain development in a spinothalamic tract‐lesion model
2022
Overview
Aims Neuropathic pain after spinal cord injury is one of the most difficult clinical problems after the loss of mobility, and pharmacological or neuromodulation therapy showed limited efficacy. In this study, we examine the possibility of pain modulation by a recombinant adeno‐associated virus (rAAV) encoding small‐hairpin RNA against GCH1 (rAAV‐shGCH1) in a spinal cord injury model in which neuropathic pain was induced by a spinothalamic tract (STT) lesion. Methods Micro‐electric lesioning was used to damage the left STT in rats (n = 32), and either rAAV‐shGCH1 (n = 19) or rAAV control (n = 6) was injected into the dorsal horn of the rats at the same time. On postoperative days 3, 7, and 14, we evaluated neuropathic pain using a behavioral test and microglial activation by immunohistochemical staining. Results A pain modulation effect of shGCH1 was observed from postoperative days 3 to 14. The mechanical withdrawal threshold was 13.0 ± 0.95 in the shGCH1 group, 4.3 ± 1.37 in the control group, and 3.49 ± 0.85 in sham on postoperative day 3 (p < 0.0001) and continued to postoperative day 14 (shGCH1 vs. control: 11.4 ± 1.1 vs. 2.05 ± 0.60, p < 0.001 and shGCH1 vs. sham: 11.4 ± 1.1 vs. 1.43 ± 0.54, p < 0.001). Immunohistochemical staining of the spinal cord dorsal horn showed deactivation of microglia in the shGCH1 group without any change of delayed pattern of astrocyte activation as in STT model. Conclusions Neuropathic pain after spinal cord injury can be modulated bilaterally by deactivating microglial activation after a unilateral injection of rAAV‐shGCH1 into the dorsal horn of a STT lesion spinal cord pain model. This new attempt would be another therapeutic approach for NP after SCI, which once happens; there is no clear curative options still now. Neuropathic pain after spinal cord injury can be modulated bilaterally by deactivating microglial activation after a unilateral injection of rAAV‐shGCH1 into the dorsal horn of a spinothalamic tract‐lesion spinal cord pain model.
Publisher
John Wiley & Sons, Inc,John Wiley and Sons Inc
Subject
/ GTP Cyclohydrolase - genetics
/ GTP Cyclohydrolase - metabolism
/ Lesions
/ Male
/ Neuralgia - prevention & control
/ Original
/ Pain
/ Rats
/ RNA, Small Interfering - genetics
/ RNA, Small Interfering - metabolism
/ Software
/ Spinal Cord Injuries - physiopathology
/ Spinothalamic Tracts - injuries
