BDNF postsynaptically modulates hippocampal synaptic transmission and plasticity (2). Activation of postsynaptic TrkB receptors by BDNF causes depolarization of the postsynaptic neuron, presumably through opening of Na+ channels (9) and concomitant activation of Ca2+ channels, resulting in an increase in the Ca2+ concentration. During synaptic transmission, postsynaptic cell depolarization caused by the activation of TrkB receptors enhances NMDA receptor opening by removing a Mg2+ block from the receptor channel, which then facilitates the induction of LTP in the postsynaptic cell.