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Journal Article
Research Support, Non-U.S. Gov't
Treatment with nerve grafts and aFGF attenuates allodynia caused by cervical root transection injuries.
PURPOSE: Nerve root traction injuries induce spinal cord inflammation and lead to neuronal death within days. In the present study, we examined the inflammatory response one week after multiple cervical root transections.
METHODS: In the transection group, the left cervical roots (C6-8) of rats were cut at the spinal cord junction. In the repair group, transected roots were repaired with nerve grafts and the subsequent application of aFGF and fibrin glue. A sham group had nerve roots exposed without transection. Mechanical allodynia and spinal glial responses were evaluated.
RESULTS: Allodynia did not differ between the treatment groups on day 2. Rats with transected spinal nerve roots had significantly more allodynia by 7 days, which was associated with IL-1β expression in dorsal and ventral horn astrocytes, and microglia activation. Repair of nerve roots with autologous intercostal nerve grafts and FGF in fibrin glue attenuated the allodynia, reduced IL-1β expression in astroctyes and reduced microglia activation, along with a significant increase in arginase I expression.
CONCLUSION: This study demonstrated a correlation between an increased number of IL-1β-positive astrocytes and the development of allodynia. Our treatment significantly decreased IL-1β-positive astrocytes, thus preventing the occurrence of neuropathic pain following multiple cervical root injuries.
METHODS: In the transection group, the left cervical roots (C6-8) of rats were cut at the spinal cord junction. In the repair group, transected roots were repaired with nerve grafts and the subsequent application of aFGF and fibrin glue. A sham group had nerve roots exposed without transection. Mechanical allodynia and spinal glial responses were evaluated.
RESULTS: Allodynia did not differ between the treatment groups on day 2. Rats with transected spinal nerve roots had significantly more allodynia by 7 days, which was associated with IL-1β expression in dorsal and ventral horn astrocytes, and microglia activation. Repair of nerve roots with autologous intercostal nerve grafts and FGF in fibrin glue attenuated the allodynia, reduced IL-1β expression in astroctyes and reduced microglia activation, along with a significant increase in arginase I expression.
CONCLUSION: This study demonstrated a correlation between an increased number of IL-1β-positive astrocytes and the development of allodynia. Our treatment significantly decreased IL-1β-positive astrocytes, thus preventing the occurrence of neuropathic pain following multiple cervical root injuries.
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