The receptor tyrosine kinase B, TrkB, is the high-affinity receptor for brain-derived neurotrophic factor (BDNF). Much evidence supports a role for TrkB signaling in excitatory synapse formation. There have been a number of recent advances in understanding the cell biology of TrkB-mediated excitatory synaptogenesis. The predominant mechanism by which TrkB supports excitatory synaptogenesis appears to be due to cell-autonomous signaling in both pre- and postsynaptic cells. This signaling appears to contribute to the growth and stabilization processes necessary for the net formation of synapses during development. Further, the molecular mechanisms by which TrkB contributes to these growth and stabilization processes are beginning to be elucidated.