21:I[432972,["/_next/static/chunks/bb923814e1f4d2e9.js","/_next/static/chunks/dd3ee9f5b7716ca6.js","/_next/static/chunks/4204a0ae82542ca8.js","/_next/static/chunks/1270dead247da766.js","/_next/static/chunks/6e1aa89a642f40be.js","/_next/static/chunks/2d7aa753e81324a8.js","/_next/static/chunks/8ffd0b71567920d8.js","/_next/static/chunks/67ea6dfd21f16c5f.js","/_next/static/chunks/24eb4379f68013fd.js","/_next/static/chunks/b8cd775ffdf935bd.js","/_next/static/chunks/983103cd9eb7b428.js","/_next/static/chunks/263f2cdcb9aa2341.js","/_next/static/chunks/294b9525248c8e5f.js"],"default"] 22:T4ba,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 Ca²⁺ influx from L-type voltage-gated Ca²⁺ 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.23:T48f,Dendrites are crucial for integrating incoming synaptic information. Individual dendritic branches are thought to constitute a signal processing unit, yet how neighboring synapses shape the boundaries of functional dendritic units is not well understood. Here, we address the cellular basis underlying the organization of the strengths of neighboring Schaffer collateral-CA1 synapses by optical quantal analysis and spine size measurements. Inducing potentiation at clusters of spines produces NMDA-receptor-dependent heterosynaptic plasticity. The direction of postsynaptic strength change shows distance dependency to the stimulated synapses where proximal synapses predominantly depress, whereas distal synapses potentiate; potentiation and depression are regulated by CaMKII and calcineurin, respectively. In contrast, heterosynaptic presynaptic plasticity is confined to weakening of presynaptic strength of nearby synapses, which requires CaMKII and the retrograde messenger nitric oxide. Our findings highlight the parallel engagement of multiple signaling pathways, each with characteristic spatial dynamics in shaping the local pattern of synaptic strengths.24:T601,

#	Concept	H-Index	Publications	Citations
1	Medicine	3	3	77
2	Social Sciences	3	3	77
3	Neuroscience	3	3	77
4	Cognitive Science	2	2	39
5	Behavioral Sciences	1	1	27

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