By Christine C. Stichel-Gunkel
Since the pioneering stories of Ramon y Cajal the lack of lesioned grownup CNS axons to regenerate has been good verified. up to now years developments in molecular, mobile and biochemical wisdom have supplied new insights into the extrinsic mechanims underlying regeneration failure. The speedy growth during this box has already resulted in the advance of recent options for healing manipulations. This booklet offers a complete assessment of structural and molecular alterations brought on by way of an invasive CNS lesion and their involvements in regeneration methods. additionally, it demonstrates the robust growth-promoting actitivies of implanted glial cells. the information is mentioned in terms of present wisdom at the mechanisms of axonal degeneration and regeneration and when it comes to their relevance for the improvement of novel healing strategies.
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Extra info for The Role of Microenvironment in Axonal Regeneration: Influences of Lesion-Induced Changes and Glial Implants on the Regeneration of the Postcommissural Fornix
Example text
1984), with the exception of some punctate intraneuronal staining (Yamamoto et al. 1988; Hagg et al. 1989; Suzuki et al. 1990; Zhou 1990; Jucker et al. 1992). The present study confirmed these previous results but, in addition, revealed some laminin-immunopositive astro48 cytes in the unlesioned adult CNS tissue. The observation that astroglial cells produce laminin in vitro (Manthorpe et al. 1983; Matthiessen et al. 1989) and the presence of laminin-mRNA in astroglial cells of embryonal and neonatal rats (Hu et al.
Tenascin-immunopositive cells and deposits were distributed within the immediate environment of the lesion site in those regions of the tract containing degenerating fibers. These results confirm previous findings in the spinal cord (Pindzola et al. 1993; Zhang et al. 1995). One step toward an understanding of the molecular link between fiber degeneration and up-regulation of tenascin was presented in the study by Ard and colleagues (1993). They found that degenerating axons are not a sufficient signal to induce re-expression of tenascin, but that other elements such as degenerating myelin, reactive microglia, or connective tissue are necessary for the induction.
D LNGFR immunostaining of neurons in the diagonal band (D,B) that serves as positive control. Large arrows indicate the location of lesion/implantation site; small arrows delineate the distal stump. 21A-F. Degeneration and demyelination of fornix fibers in an animal with Schwann cell implant at 4 days after implantation. Neurofilament (NF, A and B), myelin-associated glycoprotein (MAG, C and D), and myelin basic protein (MBP, E and F) immunostaining of serial cryostat sections revealed an area of necrosis around the lesion/implantation site.
