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. 2011 Mar 31;6(3):e18373. doi: 10.1371/journal.pone.0018373

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Blakely et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.

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Select antagonists were used to identify the downstream signaling pathway responsible for mediating the effects of Wnt5a on DA neurites. Antagonism of the canonical Wnt pathway (using Dkk1 recombinant protein), the canonical and non-canonical Wnt pathways (using casein kinase 1 inhibitor, D4476) and even more selectively the non-canonical PCP pathway (using Rac1 inhibitor, NSC23766) revealed that the effect of Wnt5a on (A) neurite length and (B) neurite number were mediated by the non-canonical PCP pathway (D4476 and NSC23766 both significantly antagonizing the effects of Wnt5a). (C–F) Examples of changes in DA neuron morphology following treatment with Wnt5a ± selective antagonists. Scale bar = 50 µm. Data represents mean ± s.e.m., n = 4–5 cultures; ** p<0.01, *** p<0.001.