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Hebbian plasticity is thought to require glutamate signalling. We show this is not the case for hippocampal presynaptic long-term potentiation (LTP pre ), which is expressed as an increase in transmitter release probability (P r ). We find that LTP pre  can be induced by pairing pre- and postsynaptic spiking in the absence of glutamate signalling. LTP pre  induction involves a non-canonical mechanism of retrograde nitric oxide signalling, which is triggered by Ca 2+  influx from L-type voltage-gated Ca 2+  channels, not postsynaptic NMDA receptors (NMDARs), and does not require glutamate release. When glutamate release occurs, it decreases P r  by activating presynaptic NMDARs, and promotes presynaptic long-term depression. Net changes in P r , therefore, depend on two opposing factors: (1) Hebbian activity, which increases P r , and (2) glutamate release, which decreases P r . Accordingly, release failures during Hebbian activity promote LTP pre  induction. Our findings reveal a novel framework of presynaptic plasticity that radically differs from traditional models of postsynaptic plasticity.

Glutamate is required for depression but not potentiation of long-term presynaptic function