• Bradley J Kerr and Samuel David.
• Centre for Research in Neuroscience, The Research Institute of the McGill University Health Centre, 1650 Cedar Ave., Montreal, Quebec, Canada H3G 1A4. bradley.kerr@ualberta.ca
• Exp. Neurol. 2007 Aug 1;206(2):240-7.

AbstractWe have characterized spontaneous and evoked pain behaviors that develop in a model of severe spinal contusion injury using two commonly used strains of mice. Using the Infinite Horizon Tissue Impactor to produce these contusion injuries, we were able to set strict limits on the injury parameters (i.e., force of impact and tissue displacement). This helps to generate a uniform population of spinal cord injury severity and allows for meaningful comparisons to be made across the two strains of mice. After contusion injury, strain differences were apparent in several injury-evoked behaviors such as hindlimb spasticity, spontaneous caudally directed nociceptive behaviors and over-grooming. Similar to the anatomical rearrangements observed in the rat after spinal cord injury, we observed significant changes in sensory innervation of the dorsal horn in both strains. In addition, there was increased expression of protein kinase C gamma (PKCgamma) in cells outside of the inner region of lamina II (IIi) in both strains after spinal contusion injury. However, the magnitude and intensity of this increase was more pronounced in BALB/c mice. PKCgamma is an important mediator of persistent pain behaviors after peripheral nerve injury and inflammation. Our results suggest that PKCgamma may also contribute to neuropathic pain behaviors after direct lesion to the spinal cord.

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