Activation of Ca2+/calmodulin-dependent protein kinase II α in the spinal cords of rats with clip compression injury

Ca2+/calmodulin-dependent protein kinase II α (CaMKIIα) is abundant in the central nervous system, where it plays important roles in regulating neuronal plasticity and survival. However, the role of CaMKIIα activation in traumatically injured spinal cords remains unclear. This study examined the effects of clip compression injury on levels of phosphorylated CaMKIIα (pCaMKIIα) and its cellular localization in rat spinal cords. Western blot analysis showed that the pCaMKIIα levels in both rostral (days 7, 14, and 21 post-injury) and caudal (days 4, 7, 14, and 21 post-injury) areas of the injury site were more than twice the levels in the non-injured controls. Immunohistochemical examination revealed constitutive localization of pCaMKIIα in the superficial lamina of the dorsal horn and neurons in normal spinal cord controls. After spinal cord injury, levels of the same components were markedly increased in both rostral and caudal regions ∼ 3 mm from the center of the spinal cord lesions. However, pCaMKIIα was very rare in inflammatory cells in the injured spinal cords. In this animal model, CaMKIIα may play an important role in the spontaneous reversal of spinal cord dysfunction, thus restoring locomotor activity, possibly by functioning in the reconstruction of synaptic transmission and in protecting neurons from spinal cord injury.