4.3 Article

Retinal TrkB receptors regulate neural development in the inner, but not outer, retina

期刊

MOLECULAR AND CELLULAR NEUROSCIENCE
卷 38, 期 3, 页码 431-443

出版社

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.mcn.2008.04.004

关键词

retina; photoreceptors; development; BDNF; TrkB; electroretinograms

资金

  1. Intramural NIH HHS [Z01 EY000415] Funding Source: Medline
  2. NEI NIH HHS [P30 EY002162, R37 EY001869, R01 EY001869, EY01919, EY06842, EY01869, F32 EY006842, K08 EY000415, R01 EY001919, R01 EY006842, EY02162] Funding Source: Medline
  3. NINDS NIH HHS [R01 NS050596, P01 NS016033-260014, P01 NS016033-26, NS16033, R56 NS050596, NS050596, P01 NS016033] Funding Source: Medline

向作者/读者索取更多资源

BDNF signaling through its TrkB receptor plays a pivotal role in activity-dependent refinement of synaptic connectivity of retinal ganglion cells. Additionally, studies using TrkB knockout mice have suggested that BDNF/TrkB signaling is essential for the development of photoreceptors and for synaptic communication between photoreceptors and second order retinal neurons. Thus the action of BDNF on refinement of synaptic connectivity of retinal ganglion cells could be a direct effect in the inner retina, or it could be secondary to its proposed role in rod maturation and in the formation of rod to bipolar cell synaptic transmission. To address this matter we have conditionally eliminated TrkB within the retina. We find that rod function and synaptic transmission to bipolar cells is not Compromised in these conditional knockout mice. Consistent with previous work, we find that inner retina neural development is regulated by retinal BDNF/TrkB signaling. Specifically we show here also that the complexity of neuronal processes of dopaminergic cells is reduced in conditional TrkB knockout mice. We conclude that retinal BDNF/TrkB signaling has its primary role in the development of inner retinal neuronal circuits, and that this action is not a secondary effect due to the loss of visual signaling in the outer retina. (C) 2008 Elsevier Inc. All rights reserved.

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