The mechanisms underlying synaptic plasticity in the hippocampus have been widely studied due to their presumed involvement in mnemonic functions in the brain. Similar mechanisms are thought to guide maturation and refinement of the neuronal circuitry; however, much less is known on the mechanisms of synaptic plasticity during early development. Immature synapses in area CA1 of rat hippocampus display a large heterogeneity in the probability of glutamate release (Pr), manifest as heterogeneity in short-term plasticity. We have recently shown that the low Pr facilitatory synapses can be rapidly converted to non-facilitatory ones by pairing afferent stimulation to postsynaptic depolarization. Thus, in contrast to the adult, immature CA3-CA1 synapses can readily regulate short-term dynamics of transmission in an activity-dependent manner (Lauri et al., Neuron, 50(3): 415, 2006). This form of presynaptic plasticity is coexpressed with the adult type LTP mechanisms at the neonate (P3-P6) CA1 and downregulated during maturation of the circuitry. The activity-dependent switch in short-term dynamics requires postsynaptic calcium signaling, implying involvement of a retrograde messenger. I'll present evidence suggesting that the brain derived neurotrophic factor (BDNF), acting via the TrkB receptors and downregulating the function of presynaptic kainate – type glutamate receptors, mediates this novel form of presynaptic plasticity at the immature CA3-CA1 synapses.