Schematic diagram summarizing the known possible TrkB signalling pathways associated with neuronal plasticity. Within neurons (dotted square), BDNF can induce three types of Trk B dimers to form: (1) TK+ homodimer; (2) heterodimer and (3) T1 homodimer. The TK+ homodimer results in activation of PLCγ and PKC, which promote synaptic plasticity. Shc proteins activate the PI3K-Akt pathway and cell survival while Ras-MAPK pathway activation regulates differentiation. The function of the heterodimer remains unknown. The T1 homodimer is important in synaptic transmission within neurons but a mechanism for this phenomena has not yet been elucidated. However, T1 is the major isoform of TrkB receptors in astrocytes (grey box), which induces release of Rho GDI1 and is involved in a influx in astrocytes. A TTIP (truncated TrkB-interacting protein) binds T1 but its functions are not yet clear. Adapted from [69].
