Baudoin Jean-Pierre, Alvarez Chantal, Gaspar Patricia, Métin Christine
INSERM, U839, Hôpital Pitié-Salpêtrière, Paris, France.
Dev Neurosci. 2008;30(1-3):132-43. doi: 10.1159/000109858.
We have shown previously that actomyosin contractility plays an important role in controlling nuclear movements in future interneurons born in the medial ganglionic eminence (MGE) [Bellion et al.: J Neurosci 2005;25:5691-5699]. Because microtubules are known to control the structural and motile properties of migrating neurons, we asked whether alterations in the dynamic instability of microtubules would impair MGE cell migration. Migration was analyzed in flat cocultures in which green-fluorescent-protein-expressing MGE cells migrate on cortical cells from their explant of origin. A low (100 nM) concentration of nocodazole shortened the leading process of MGE cells that nevertheless continued to migrate at the same rate but frequently changed their direction of migration relative to control cells. MGE cells treated with a higher (1 muM) concentration of nocodazole that strongly destabilized microtubules took on multipolar morphology. They extended thin and labile processes. MGE cells no longer exhibited directional migration and migration velocity slowed 2-fold. These results suggest that microtubule stability is crucial for maintaining polarity and controlling the directional migration of MGE cells, whereas additional mechanisms are required to control cell motility.
我们之前已经表明，肌动球蛋白收缩性在控制内侧神经节隆起（MGE）中新生的未来中间神经元的核运动中起着重要作用[贝里昂等人：《神经科学杂志》2005年；25:5691 - 5699]。由于已知微管控制迁移神经元的结构和运动特性，我们询问微管动态不稳定性的改变是否会损害MGE细胞迁移。在扁平共培养物中分析迁移情况，其中表达绿色荧光蛋白的MGE细胞从其起源外植体在皮质细胞上迁移。低浓度（100 nM）的诺考达唑缩短了MGE细胞的前端突起，不过这些细胞仍以相同速率继续迁移，但相对于对照细胞，其迁移方向频繁改变。用较高浓度（1 μM）的诺考达唑处理MGE细胞，这种处理会强烈破坏微管的稳定性，结果这些细胞呈现多极形态。它们伸出细而不稳定的突起。MGE细胞不再表现出定向迁移，迁移速度减慢了2倍。这些结果表明，微管稳定性对于维持MGE细胞的极性和控制其定向迁移至关重要，而控制细胞运动性还需要其他机制。
