| First Author | Padamsey Z | Year | 2017 |
| Journal | Elife | Volume | 6 |
| PubMed ID | 29140248 | Mgi Jnum | J:254989 |
| Mgi Id | MGI:6110932 | Doi | 10.7554/eLife.29688 |
| Citation | Padamsey Z, et al. (2017) Glutamate is required for depression but not potentiation of long-term presynaptic function. Elife 6:e29688 |
| abstractText | Hebbian plasticity is thought to require glutamate signalling. We show this is not the case for hippocampal presynaptic long-term potentiation (LTPpre), which is expressed as an increase in transmitter release probability (Pr). We find that LTPpre can be induced by pairing pre- and postsynaptic spiking in the absence of glutamate signalling. LTPpre 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 Pr by activating presynaptic NMDARs, and promotes presynaptic long-term depression. Net changes in Pr, therefore, depend on two opposing factors: (1) Hebbian activity, which increases Pr, and (2) glutamate release, which decreases Pr. Accordingly, release failures during Hebbian activity promote LTPpre induction. Our findings reveal a novel framework of presynaptic plasticity that radically differs from traditional models of postsynaptic plasticity. |
