1. Institute of Neuroscience, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China
2. Graduate School of the Chinese Academy of Sciences, Shanghai 200031, China
3. These authors contributed equally to this work

Correspondence to: Yi-zheng Wang¹Xiao-bing Yuan¹ Correspondence and requests for materials should be addressed to X.-b.Y. (Email: yuanxb@ion.ac.cn) or Y.-z.W. (Email: yzwang@ion.ac.cn).

Abstract

Brain-derived neurotrophic factor (BDNF) is known to promote neuronal survival and differentiation¹ and to guide axon extension both in vitro ^{2, 3} and in vivo ⁴. The BDNF-induced chemo-attraction of axonal growth cones requires Ca²⁺ signalling³, but how Ca²⁺ is regulated by BDNF at the growth cone remains largely unclear. Extracellular application of BDNF triggers membrane currents resembling those through TRPC (transient receptor potential canonical) channels in rat pontine neurons⁵ and in Xenopus spinal neurons⁶. Here, we report that in cultured cerebellar granule cells, TRPC channels contribute to the BDNF-induced elevation of Ca²⁺ at the growth cone and are required for BDNF-induced chemo-attractive turning. Several members of the TRPC family are highly expressed in these neurons, and both Ca²⁺ elevation and growth-cone turning induced by BDNF are abolished by pharmacological inhibition of TRPC channels, overexpression of a dominant-negative form of TRPC3 or TRPC6, or downregulation of TRPC3 expression via short interfering RNA. Thus, TRPC channel activity is essential for nerve-growth-cone guidance by BDNF.

1. Institute of Neuroscience, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China
2. Graduate School of the Chinese Academy of Sciences, Shanghai 200031, China
3. These authors contributed equally to this work

Correspondence to: Yi-zheng Wang¹Xiao-bing Yuan¹ Correspondence and requests for materials should be addressed to X.-b.Y. (Email: yuanxb@ion.ac.cn) or Y.-z.W. (Email: yzwang@ion.ac.cn).

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