Adult human and rodent brains contain neural stem and progenitor cells, and the presence of neural stem cells in the adult rodent spinal cord has also been described. Here, using electron microscopy, expression of neural precursor cell markers, and cell culture, we investigated whether neural precursor cells are also present in adult human spinal cord. In well-preserved nonpathological post-mortem human adult spinal cord, nestin, Sox2, GFAP, CD15, Nkx6.1, and PSA-NCAM were found to be expressed heterogeneously by cells located around the central canal. Ultrastructural analysis revealed the existence of immature cells close to the ependymal cells, which display characteristics of type B and C cells found in the adult rodent brain subventricular region, which are considered to be stem and progenitor cells, respectively. Completely dissociated spinal cord cells reproducibly formed Sox2(+) nestin(+) neurospheres containing proliferative precursor cells. On differentiation, these generate glial cells and gamma-aminobutyric acid (GABA)-ergic neurons. These results provide the first evidence for the existence in the adult human spinal cord of neural precursors with the potential to differentiate into neurons and glia. They represent a major interest for endogenous regeneration of spinal cord after trauma and in degenerative diseases.
and Frédérique Scamps. Axotomy-induced expression of calciumactivated chloride current in subpopulations of mouse dorsal root ganglion neurons. J Neurophysiol 90: 3764 -3773, 2003. First published August 27, 2003 10.1152/jn.00449.2003. Whole cell patchclamp recordings of calcium-activated chloride current [I Cl(Ca) ] were made from adult sensory neurons of naive and axotomized mouse L 4 -L 6 lumbar dorsal root ganglia after 1 day of culture in vitro. A basal I Cl(Ca) was specifically expressed in a subset of naive mediumdiameter neurons (30 -40 m). Prior nerve injury, induced by sciatic nerve transection 5 days before experiments, increased both I Cl(Ca) amplitude and its expression in medium-diameter neurons. Moreover, nerve injury also induced I Cl(Ca) expression in a new subpopulation of neurons, the large-diameter neurons (40 -50 m). Small-diameter neurons (inferior to 30 m) never expressed I Cl(Ca) . Regulated I Cl(Ca) expression was strongly correlated with injury-induced regenerative growth of sensory neurons in vitro and nerve regeneration in vivo. Cell culture on a substrate not permissive for growth, D,L-polyornithine, prevented both elongation growth and I Cl(Ca) expression in axotomized neurons. Regenerative growth and the induction of I Cl(Ca) expression take place 2 days after injury, peak after 5 days of conditioning in vivo, slowly declining thereafter to control values. The selective expression of I Cl(Ca) within medium-and large-diameter neurons conditioned for rapid, efficient growth suggests that these channels play a specific role in postinjury behavior of sensory neuron subpopulations such as neuropathic pain and/or axonal regeneration.
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