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Fig. 4. The induction of filopodia by TrkB.T1 is independent from ligand binding, TrkB kinase activity, and from the intracellular domain of TrkB.T1. (A) Hippocampal neurons were transfected with TrkB.T1-GFP, TrkB.FL-GFP or GFP expression plasmids. On the day of transfection, either TrkB ligand (BDNF or NT-4/5) was added (100 ng/ml), or endogenously released ligand was scavenged with TrkB-Fc receptor bodies (0.4 µg/ml). The density of filopodia was determined 2 days later. Neither exogenous application of ligand nor scavenging of endogenously released ligands with TrkB-Fc receptor bodies influenced the density of dendritic filopodia (n=10-50 cells; two to five independent experiments, ^*P<10^–4, compared with TrkB.T1-GFP positive control). (B) K252a (200 nM), did not affect the growth of filopodia, indicating the lack of an effect of Trk kinase signalling. ^*Significantly different from TrkB.T1-GFP with P<0.05. (C) The induction of filopodia by a deletion mutant of TrkB.T1 without intracellular domain (T1 ${Delta}$ ICD-GFP) was not significantly different (P>0.14) from the TrkB.T1-GFP-induced effect. The increase in filopodia caused by T1 ${Delta}$ ICD-GFP is statistically significant compared to TrkB.FL-GFP transfected controls (^*P<0.05, n=8-26 cells).

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