| First Author | Pollock GS | Year | 2003 |
| Journal | J Neurosci | Volume | 23 |
| Issue | 31 | Pages | 10137-45 |
| PubMed ID | 14602830 | Mgi Jnum | J:88208 |
| Mgi Id | MGI:3029671 | Doi | 10.1523/JNEUROSCI.23-31-10137.2003 |
| Citation | Pollock GS, et al. (2003) TrkB receptor signaling regulates developmental death dynamics, but not final number, of retinal ganglion cells. J Neurosci 23(31):10137-45 |
| abstractText | We investigated the effects of endogenous neurotrophin signaling on the death-survival of immature retinal ganglion cells (RGCs) in vivo. Null mutation of brain-derived neurotrophic factor [(BDNF) alone or in combination with neurotrophin 4 (NT4)] increases the peak rate of developmental RGC death as compared with normal. Null mutation of NT4 alone is ineffective. Null mutation of the full-length trkB (trkBFL) receptor catalytic domain produces a dose-dependent increase in the peak RGC death rate that is negatively correlated with retinal levels of trkBFL protein and phosphorylated (activated) trkBFL. Depletion of target-derived trkB ligands by injection of trkB-Fc fusion protein into the superior colliculus increases the peak rate of RGC death compared with trkA-Fc-treated and normal animals. Adult trkBFL+/- mice have a normal number of RGCs, despite an elevated peak death rate of immature RGCs. Thus, target-derived BDNF modulates the dynamics of developmental RGC death through trkBFL activation, but BDNF/trkB-independent mechanisms determine the final number of RGCs. |
