Changes in CaMKIIα expression in spinal cord and dorsal root ganglia during remifentanil-induced hyperalgesia in a rat model of incisional pain

Objective To investigate the changes in the expression of Ca2+ /calmodulin-dependent protein kinaseⅡα(CaMKⅡα)in the spinal cord and dorsal root ganglia(DRG) during remifentanil-induced hyperalgesia in a rat model of incisional pain(IP). Methods Thirty-two male Sprague-Dawley rats in which caudal vein catheter was successfully placed, aged 260-280 g, were divided into 4 groups(n=8 each) using a random number table method: control group(group C), IP group, remifentanil group(group R)and remifentanil plus IP group(group RIP). Normal saline was infused via the caudal vein for 60 min at a rate of 0.1 ml·kg-1·min-1 in group C. Normal saline was infused via the caudal vein for 60 min at a rate of 0.1 ml·kg-1·min-1, and the model of IP was simultaneously established in group IP. Remifentanil was infused via the caudal vein for 60 min at a rate of 1.0 μg· kg-1·min-1 in group R. Remifentanil was infused via the caudal vein for 60 min at a rate of 1.0 μg· kg-1·min-1, and the model of IP was simultaneously established in group RIP. Mechanical paw withdrawal threshold(MWT)and thermal paw withdrawal latency(TWL) were measured at 24 h before infusion and 2, 6, 24 and 48 h after infusion(T0-4). The rats were sacrificed after the last behavioral test, and L4-6 segment of the spinal cord and DRGs were removed for determination of the expression of total and phosphorylated CaMKⅡα (tCaMKⅡα, pCaMKⅡα) by Western blot.The ratio of pCaMKⅡα/tCaMKⅡα was calculated. Results Compared with group C, MWT was significantly decreased, TWL was shortened, the expression of tCaMKⅡα and pCaMKⅡα in the spinal cord and DRGs was up-regulated, and the ratio of pCaMKⅡα/tCaMKⅡα was increased in I, R and RIP groups(P<0.05 or 0.01). Compared with group IP and group R, MWT was significantly decreased, TWL was shortened, the expression of tCaMKⅡα and pCaMKⅡα in the spinal cord and DRGs was up-regulated, and the ratio of pCaMKⅡα/tCaMKⅡα was increased in group RIP (P<0.05 or 0.01). Conclusion The mechanism by which remifentanil induces hyperalgesia may be related to up-regulated expression of CaMKⅡα in the spinal cord and DRGs in a rat model of IP. Key words: Piperidines; Hyperalgesia; Pain, postoperative; Calcium-calmodulin-dependent protein kinases; Spinal cord; Ganglia, spinal