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The p75 neurotrophin receptor mediates the TrkBT1 receptor induced outgrowth of dendritic filopodia in hippocampal neurons


, : The p75 neurotrophin receptor mediates the TrkBT1 receptor induced outgrowth of dendritic filopodia in hippocampal neurons. Society for Neuroscience Abstract Viewer & Itinerary Planner : Abstract No 334 4

The Trk kinases and the p75 receptor (p75NTR) mediate the effects of neurotrophins on neuronal survival, differentiation and synaptic plasticity. The neurotrophin BDNF and its cognate receptor, TrkB.FL, are highly expressed in CNS neurons. Later during postnatal development the truncated TrkB splice variants (TrkB.T1, TrkB.T2) are abundantly expressed in the CNS. However, the signaling mechanisms of these truncated receptors remained elusive. Here we show that overexpression of TrkB.T1 in hippocampal neurons induces the formation of dendritic filopodia. Microcultures of postnatal rat hippocampal neurons were transfected at 8 DIV with expression plasmids coding for TrkB.T1-GFP, and actin containing dendritic filopodia were quantified 3 days later.TrkB.T1 induced the formation of 6.8 +- 0.9 filopodia per 40 mum dendritic length compared to 2.9 +- 0.6 in controls (p<10-5). This effect was independent of neurotrophin binding and was also seen with a mutant TrkB.T1 that lacked the cytoplasmic tail. Coexpression of TrkB.FL had a dominant negative effect on TrkB.T1 induced filopodial growth. Incubation with a neutral sphingomyelinase inhibitor (3 muM spiroepoxide) and with a p75 extracellular epitope antibody (MC192, 8 mug/ml), indicated that the TrkB.T1 effect was mediated by the p75NTR, and subsequent activation of ceramide production. Intriguingly, the TrkB.T1 induced growth of dendritic filopodia was inhibited by coexpression of a dominant negative p75NTR which lacks the cytoplasmic domain, thus supporting signaling of TrkB.T1 via p75NTR.We thus propose a novel signaling pathway initiated by interaction of TrkB.T1 with the p75NTR receptor in the absence of neurotrophins, which modulates dendritic growth via p75NTR signaling cascades. This mechanism could be involved in the generation of synaptic spines.

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