日本奈良尖端科学技术大学院大学、东北大学等机构的研究人员12日报告说，他们通过动物实验，发现了神经细胞轴突形成的机制。
轴突是神经细胞长出的一根较长的圆柱形细长突起，每个正常的神经细胞只会伸出一个轴突。它是神经系统主要的信号传递通道，人类的轴突最长可以达到1米。
此前，研究人员已知轴突的前端是通过扩展细胞膜而伸长的，但是一直不清楚其详细的形成机制。新研究中，奈良尖端科学技术大学院大学副教授稻垣直之等人利用大鼠脑神经细胞进行实验，发现细胞内的一种蛋白质“Rab33a”会将合成细胞膜的成分运到轴突前端，从而使轴突向前生长。
研究人员还发现，如果减少“Rab33a”蛋白质的量，轴突形成就减缓，如果这种蛋白质过量，则细胞膜成分的供应过剩，一个神经细胞会长出多条轴突。
这一研究成果已发表在新一期《神经科学杂志》上。稻垣直之认为，新发现将有助于治疗脊髓损伤等疾病，在再生医疗领域得到应用。（生物谷Bioon.com）
doi: 10.1523/JNEUROSCI.0989-12.2012
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Rab33a Mediates Anterograde Vesicular Transport for Membrane Exocytosis and Axon Outgrowth
Hitomi Nakazawa, Tadayuki Sada, Michinori Toriyama, Kenji Tago, Tadao Sugiura, Mitsunori Fukuda, and Naoyuki Inagaki
Axon outgrowth requires plasma membrane expansion, which results from post-Golgi vesicular transport and fusion. However, the molecular mechanisms regulating post-Golgi vesicular trafficking for membrane expansion and axon outgrowth remain unclear. Here, we show that Rab33a expression became upregulated during axon outgrowth of cultured rat hippocampal neurons. Rab33a was preferentially localized to the Golgi apparatus and to synaptophysin-positive vesicles that are transported along the growing axon. Previous studies showed that synaptophysin is localized to post-Golgi vesicles transported by fast axonal transport in developing neurons. Reduction of Rab33a expression by RNAi (RNA interference) inhibited the anterograde transport of synaptophysin-positive vesicles, leading to their decrease in axonal tips. Furthermore, this treatment reduced membrane fusion of synaptophysin-positive vesicles at the growth cones and inhibited axon outgrowth. Overexpression of Rab33a, on the other hand, induced excessive accumulation of synaptophysin-positive vesicles and concurrent formation of surplus axons. These data suggest that Rab33a participates in axon outgrowth by mediating anterograde axonal transport of synaptophysin-positive vesicles and their concomitant fusion at the growth cones.
