Bcl-x(L) increases axonal numbers but not axonal elongation from rat retinal explants
Gunnar P H Dietz1, Birgit Dietz, Mathias Bähr
1DFG Research Center for Molecular Physiology of the Brain (CMPB), Neurologische Universitätsklinik, Waldweg 33, 37073 Göttingen, Germany. gdietz@gwdg.de
Abstract:
The Bcl-2 family of proteins has been characterized as a key regulator of cell death programs. In addition, these proteins also play important roles in cellular differentiation, such as axonal growth. The role of Bcl-2 family members on axonal regeneration and neurite extension has been controversial so far. Here, we examine the influence of Bcl-x(L) on axonal regeneration from adult retina explants in vitro. We delivered recombinant Bcl-x(L) into retinal tissue, mediated by the Tat-protein transduction domain, and observed its effect on retinal axon extension. We found that Bcl-x(L) increased the number of regenerating neurites, but did not increase their length. Our results indicate that Bcl-x(L) stimulates axonal initiation but not axonal elongation after crush injury to retinal explants, without altering the number of surviving neurons.


