Evaluation of TNF-α and IL-6 Release in the Ventroposterolateral Nucleus of the Thalamus during Central Neuropathic Pain Induced by Electrical Injury of the Spinothalamic Tract in Male Rats: A Microdialysis Study

Inflammation and proinflammatory cytokines play an important role in the initiation and maintenance of central neuropathic pain. There are several reports that cytokine production is increased at the lesion site following spinal injury. A few studies have investigated the supraspinal levels of these cytokines. This study intended to determine TNF-α and IL-6 release in the ventroposterolateral nucleus of the thalamus in spinal cord injury-related neuropathic pain in rats.

Male Sprague-Dawley rats that weighed 200-230 g were used. Following administration of anesthesia, spinothalamic tract injury was performed by a laminectomy at the T9-T10 level in male rats. Mechanical allodynia and motor performance were evaluated at 3, 7, 14, 21 and 28 days after spinal injury by Von Frey filament and the open field test, respectively, in the sham and lesion groups. Concentrations of TNF-α and IL-6 in the VPL microdialysate were detected by ELISA in both spinal cord injured and sham groups during four weeks after surgery.

Mechanical pain threshold reduced in both hind paws following lateral spinothalamic tract injury. Paw withdrawal threshold in the Spinothalamic tract-injured group was significantly (P<0.05) lower than in sham group at day 14 post-surgery. Motor performance did not show any significant change after surgery. In the microdialysate, TNF-α reduced significantly (P<0.05) at days 3 and 7 post-injury compared to the sham group which returned to a level close to the pre-surgery level. VPL concentration of IL-6 increased significantly (P<0.05) at day 21 post-injury compared to the sham group.

Lesions in spinal pathways that contain afferent pain fibers appear to change the supraspinal levels of inflammatory mediators, including VPL, concentrations of TNF-α and IL-6 which are consistent with spinal injury related pain behavior. Cytokine production results in hyperexcitability of the thalamocortical neurons, a decrease in pain threshold, and persistent neuropathic pain after spinal injury.