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

• DOI: 10.7554/elife.29688
• Publication Date: 2017-11-15T13:00:10Z
• Authors: Zahid Padamsey; Rudi Tong; Nigel Emptage
• Keywords: Long-term depression; Postsynaptic density; Hebbian theory; Retrograde signaling; Post-tetanic potentiation; Nonsynaptic plasticity

Hebbian plasticity is thought to require glutamate signalling. We show this not the case for hippocampal presynaptic long-term potentiation (LTPpre), which expressed as an increase in transmitter release probability (Pr). find that LTPpre can be induced by pairing pre- and postsynaptic spiking absence of induction involves a non-canonical mechanism retrograde nitric oxide signalling, triggered Ca2+ influx from L-type voltage-gated channels, NMDA receptors (NMDARs), does release. When occurs, it decreases Pr activating NMDARs, promotes depression. Net changes Pr, therefore, depend on two opposing factors: (1) activity, increases (2) release, Pr. Accordingly, failures during activity promote induction. Our findings reveal novel framework radically differs traditional models plasticity.