| Autor: |
Yasufumi Hayano, Kensuke Sasaki, Nami Ohmura, Makoto Takemoto, Yurie Maeda, Toshihide Yoamashita, Yoshi Hata, Kazuhiro Kitada, Nobuhilo Yamamoto |
| Předmět: |
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| Zdroj: |
Proceedings of the National Academy of Sciences of the United States of America; 10/21/2014, Vol. 111 Issue 42, p15226-15231, 6p |
| Abstrakt: |
Axon branching is remodeled by sensory-evoked and spontaneous neuronal activity. However, the underlying molecular mechanism is largely unknown. Here, we demonstrate that the netrin family member netrin-4 (NTN4) contributes to activity-dependent thalamocortical (TC) axon branching. In the postnatal developmental stages of rodents, ntn4 expression was abundant in and around the TC recipient layers of sensory cortices. Neuronal activity dramatically altered the ntn4 expression level in the cortex in vitro and in vivo. TC axon branching was promoted by exogenous NTN4 and suppressed by depletion of the endogenous protein. Moreover, unc-5 homolog B (Unc5B), which strongly bound to NTN4, was expressed in the sensory thalamus, and knockdown of Unc5B in thalamic cells markedly reduced TC axon branching. These results suggest that NTN4 acts as a positive regulator for TC axon branching through activity-dependent expression. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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