日本奈良尖端科學(xué)技術(shù)大學(xué)院大學(xué)日前發(fā)表公報稱,，該機(jī)構(gòu)研究人員在動物實(shí)驗(yàn)中,，弄清了神經(jīng)細(xì)胞在生長過程中出現(xiàn)非對稱形狀的詳細(xì)機(jī)制，這一發(fā)現(xiàn)將有助于開發(fā)恢復(fù)受損神經(jīng)的新治療方法,。
神經(jīng)細(xì)胞本來呈球狀,，但是在生長過程中，會伸出3至6個左右的突起,，其中一個突起會變長,，成為軸突。軸突主要作用是連接其他神經(jīng)細(xì)胞,，從而使神經(jīng)細(xì)胞間可以傳遞信息,。
通過培養(yǎng)老鼠腦內(nèi)的海馬體神經(jīng)細(xì)胞，研究人員發(fā)現(xiàn),，在海馬體神經(jīng)細(xì)胞本體和突起間往來移動的“SHOOTIN”蛋白質(zhì)對于破壞神經(jīng)細(xì)胞的對稱性發(fā)揮了重要作用,。此外，如果一個突起的“SHOOTIN”蛋白質(zhì)的量比其他突起多,，那么這個突起就會伸長，最終成長為軸突,。
公報說,，研究人員今后可研究利用“SHOOTIN”蛋白質(zhì),，對脊髓損傷等神經(jīng)損傷類患者進(jìn)行治療，延長他們的神經(jīng)細(xì)胞軸突,，從而重新準(zhǔn)確連接受損或被切斷的神經(jīng),。
有關(guān)研究成果已發(fā)表在新一期英國《分子系統(tǒng)生物學(xué)》雜志網(wǎng)絡(luò)版上。（生物谷Bioon.com）
生物谷推薦原文出處：
Molecular Systems Biology doi:10.1038/msb.2010.51
A diffusion-based neurite length-sensing mechanism involved in neuronal symmetry breaking
Michinori Toriyama1, Yuichi Sakumura2,3, Tadayuki Shimada1, Shin Ishii2,3,4,5 & Naoyuki Inagaki1,3
1Graduate School of Biological Sciences, Nara Institute of Science and Technology, Ikoma, Japan
2Graduate School of Information Science, Nara Institute of Science and Technology, Ikoma, Japan
3Institute for Bioinformatics Research and Development, Japan Science and Technology Agency (JST), Tokyo, Japan
4Graduate School of Informatics, Kyoto University, Uji, Japan
5Computational Science Research Program, RIKEN, Saitama, Japan
Although there has been significant progress in understanding the molecular signals that change cell morphology, mechanisms that cells use to monitor their size and length to regulate their morphology remain elusive. Previous studies suggest that polarizing cultured hippocampal neurons can sense neurite length, identify the longest neurite, and induce its subsequent outgrowth for axonogenesis. We observed that shootin1, a key regulator of axon outgrowth and neuronal polarization, accumulates in neurite tips in a neurite length-dependent manner; here, the property of cell length is translated into shootin1 signals. Quantitative live cell imaging combined with modeling analyses revealed that intraneuritic anterograde transport and retrograde diffusion of shootin1 account for its neurite length-dependent accumulation. Our quantitative model further explains that the length-dependent shootin1 accumulation, together with shootin1-dependent neurite outgrowth, constitutes a positive feedback loop that amplifies stochastic fluctuations of shootin1 signals, thereby generating an asymmetric signal for axon specification and neuronal symmetry breaking.
