Friday, October 28, 2011
Hall 1-2 (San Jose Convention Center)
Chronic pain is a complication of many diseases like cancer, arthritis, multiple sclerosis, and diabetes. Peripheral nerve injury often leads to chronic pain symptoms. Chronic constriction injury of the sciatic nerve (CCI) is an animal model of chronic pain that has been well-characterized to produce cellular signaling changes within pain relevant regions of the spinal cord. Recent evidence shows that ependymal stem/progenitor cells (epSPCs) are found within the non-pathological spinal cord as a subpopulation of quiscent cells in the ependymal zone lining the central canal. EpSPCs have been observed to ‘awaken’ and migrate from the ependymal zone to dorsal spinal cord regions following direct spinal injury. However, whether epSPCs activate and migrate to pain-relevant dorsal spinal cord sites following localized peripheral nerve injury is entirely unknown. Nestin expression is a reliable epSPC marker. In transgenic mice, the nestin promoter drives the expression of the Cre-recombinase-modified estrogen receptor (CreERT2) fusion protein in spinal epSPCs. On administration of the estrogen congenor, Tamoxifen (TAM), CreERT2 recombines DNA loxP sites, allowing yellow fluorescent protein (YFP) expression in nestin expressing cells (‘awakened’ epSPC). Inducible nestin CreERT2 transgenic mice will be used to label, track and phenotype cells and their progeny in the adult ependymal layer of the spinal central canal. In this mouse model, we will explore whether adult-generated neurons are derived from the nestin lineage in chronic CCI-induced neuropathic mice. Immunohistochemical analysis will be done to identify YFP in specific spinal and brain regions following YFP quantification.