视网膜内核层中的细胞死亡受脑源性神经营养因子（BDNF）调控。

Cell death in the inner nuclear layer of the retina is modulated by BDNF.

作者信息

Cusato Karen, Bosco Alejandra, Linden Rafael, Reese Benjamin E

机构信息

Instituto de Biofísica, UFRJ, CCS, bloco G, Cidade Universitária, Rio de Janeiro, 21949-900, Brazil.

出版信息

Brain Res Dev Brain Res. 2002 Dec 15;139(2):325-30. doi: 10.1016/s0165-3806(02)00570-9.

DOI:10.1016/s0165-3806(02)00570-9

PMID:12480149

Abstract

Developing amacrine cells in the vertebrate retina undergo naturally-occurring cell death which is accentuated by the early removal of retinal ganglion cells. We show that providing BDNF or decreasing endogenous BDNF via competitive binding with soluble TrkB receptors in a whole-retina culture assay modulates the frequency of dying cells in the amacrine cell layer. Ganglion cells synthesize BDNF, and amacrine cells express TrkB receptors, suggesting a likely signaling mechanism.

摘要

脊椎动物视网膜中正在发育的无长突细胞会经历自然发生的细胞死亡，而早期去除视网膜神经节细胞会加剧这种死亡。我们发现在全视网膜培养试验中，通过与可溶性TrkB受体竞争性结合来提供BDNF或降低内源性BDNF，可调节无长突细胞层中死亡细胞的频率。神经节细胞合成BDNF，无长突细胞表达TrkB受体，这提示了一种可能的信号传导机制。