Endogenous pain modulation: The effects of sympathectomy on mechanical allodynia, and galanin expression in a rat model of neuropathic pain

Abstract

The sympathetic nervous system can affect the severity of neuropathic pain caused by peripheral nerve injuries. Behavioral and electrophysiological studies have demonstrated that galanin inhibits the transmission of nociceptive information in the spinal cord. The aims of the present study were to investigate the effect of surgical lumbar sympathectomy on mechanical allodynia and the expression of galanin in DRG and spinal cord (DH cells) of rats after nerve injury. We used chronic constriction injury model (CCI) to induce injury and van Frey Filaments for measuring mechanical allodynia. Surgical sympathectomy was performed by removing the sympathetic chains bilaterally from L2 to L6 levels at 10 days after CCI. Mechanical allodynia was measured using von Frey Filaments at the following time points: before CCI, 5 and 10 days after CCI, and 5 days after sympathectomy. Our result show that, the mechanical threshold for paw-withdrawal was significantly reduced at 10 and 15 days post injury (P<0.001, one-way ANOVA). Interestingly, sympathectomy did not influence the threshold on normal (control) rats; however, it did increase that of injured (CCI) rats significantly (1.08g to 4.0 g, P<0.006). Moreover, galanin immuno-staining density in the dorsal horn of the spinal cord, which increased significantly after CCI, decreased significantly after sympathectomy. However, the number of galanin immunoreactive neurons in the dorsal root ganglia (DRG), which increased after CCI, was not significantly altered after sympathectomy. Our results confirm our clinical observation that sympathectomy might be beneficial for the treatment of neuropathic pain condition such as causalgia (CRPS II). Furthermore, there seems to be an interaction between the sympathetic nervous system and the expression of galanin. However, further studies are needed to clarify this interaction.