WHY DO MATURE CNS NEURONS OF MAMMALS FAIL TO REESTABLISH CONNECTIONS FOLLOWING INJURY - FUNCTIONS OF BCL-2

Citation
Df. Chen et S. Tonegawa, WHY DO MATURE CNS NEURONS OF MAMMALS FAIL TO REESTABLISH CONNECTIONS FOLLOWING INJURY - FUNCTIONS OF BCL-2, Cell death and differentiation, 5(10), 1998, pp. 816-822
Citations number
50
Categorie Soggetti
Biology,"Cell Biology
ISSN journal
13509047
Volume
5
Issue
10
Year of publication
1998
Pages
816 - 822
Database
ISI
SICI code
1350-9047(1998)5:10<816:WDMCNO>2.0.ZU;2-F
Abstract
Factors inside and outside neurons control the process of axonal growt h and regeneration. Recently, it has become apparent that neurons are determined intrinsically for their ability to grow axons, In the mamma lian CNS, the intrinsic machinery of neurons that triggers the growth of axons during early embryonic stages is shut down at a certain point in development; as a consequence, axon elongation and regeneration ca nnot occur in postnatal life. The protooncogene Bcl-2 has been recogni zed to act as a key regulator for the program of axon elongation insid e neurons, However, expressing the gene Bcl-2 in CNS neurons is not su fficient to induce nerve regeneration in the adult CNS, eliminating th e inhibitory mechanism in the mature CNS environment is still required . Recently, the formation of glia scar has been reported to be the maj or limiting factor in the CNS environment that blocks nerve regenerati on. These new discoveries challenge the classical view of nerve regene ration in the mammalian CNS. It opens up a new dimension in the study of the cellular and molecular mechanisms underlying neurodevelopmental and neurodegenerative diseases.