Cellular and molecular neurobiology
-
Cell. Mol. Neurobiol. · Nov 2011
IT delivery of ChABC modulates NG2 and promotes GAP-43 axonal regrowth after spinal cord injury.
Chondroitin sulphate proteoglycans (CSPGs) with the major component NG2 have an inhibitory effect on regeneration of damaged axons after spinal cord injury. In this study, we investigate whether the digestion of CSPGs by chondroitinase ABC (ChABC) may decrease the NG2 expression and promote axon regrowth through the lesion site. Rats underwent spinal cord compression injury and were treated with ChABC or vehicle through an intrathecal catheter delivery at 2, 3, and 4 days after injury. ⋯ Longitudinally oriented and disorganized GAP-43-labeled axons were able to infiltrate and penetrate damaged tissue. The outgrowth of GAP-43 axons after CHABC delivery was significantly longer (≤0.457 mm) when compared with the length of axons in vehicle-treated rats (≤0.046 mm). Present findings suggest that degradation of NG2 with acute IT ChABC treatment may promote ongoing (long-lasting) axonal regenerative processes at late survival (14 and 28 days), but with no significant impact on the improvement of motor function.
-
Cell. Mol. Neurobiol. · Nov 2011
Neuregulin-1β prevents Ca(2+) overloading and apoptosis through PI3K/Akt activation in cultured dorsal root ganglion neurons with excitotoxicity induced by glutamate.
Neuregulin (NRG) plays an important role on the genesis and differentiation of neurons in the dorsal root ganglion (DRG). Whether NRG-1β regulates Ca(2+) homeostasis and apoptosis of cultured DRG neurons with excitotoxicity induced by Glu remains unknown. In this study, primary cultured DRG neurons were used to determine the effects of NRG-1β on Ca(2+) overload and apoptosis of DRG sensory neurons with excitotoxicity induced by Glu. ⋯ These effects could be inhibited by the presence of NRG-1β. The effects of NRG-1β could be blocked by PI3K inhibitor LY294002. These results implicated that NRG-1β could prevents Ca(2+) overload and apoptosis by activating PI3K/Akt pathway of primary cultured DRG neurons with excitotoxicity induced by Glu.