Greka Anna, Navarro Betsy, Oancea Elena, Duggan Anne, Clapham David E
Howard Hughes Medical Institute, Children's Hospital and Harvard Medical School, Enders 1309, 320 Longwood Avenue, Boston, Massachusetts 02115, USA.
Nat Neurosci. 2003 Aug;6(8):837-45. doi: 10.1038/nn1092.
Growth cone motility is regulated by both fast voltage-dependent Ca2+ channels and by unknown receptor-operated Ca2+ entry mechanisms. Transient receptor potential (TRP) homomeric TRPC5 ion channels are receptor-operated, Ca2+-permeable channels predominantly expressed in the brain. Here we show that TRPC5 is expressed in growth cones of young rat hippocampal neurons. Our results indicate that TRPC5 channel subunits interact with the growth cone-enriched protein stathmin 2, are packaged into vesicles and are carried to newly forming growth cones and synapses. Once in the growth cone, TRPC5 channels regulate neurite extension and growth-cone morphology. Dominant-negative TRPC5 expression allowed significantly longer neurites and filopodia to form. We conclude that TRPC5 channels are important components of the mechanism controlling neurite extension and growth cone morphology.
生长锥的运动受快速电压依赖性Ca2+通道以及未知的受体操纵性Ca2+内流机制的调节。瞬时受体电位（TRP）同聚体TRPC5离子通道是受体操纵性、Ca2+可渗透的通道，主要在大脑中表达。在此我们表明，TRPC5在幼鼠海马神经元的生长锥中表达。我们的结果表明，TRPC5通道亚基与生长锥富集蛋白stathmin 2相互作用，被包装到囊泡中，并被运输到新形成的生长锥和突触。一旦进入生长锥，TRPC5通道就会调节神经突的延伸和生长锥的形态。显性负性TRPC5的表达使神经突和丝状伪足明显更长。我们得出结论，TRPC5通道是控制神经突延伸和生长锥形态机制的重要组成部分。
