Journal
NATURE COMMUNICATIONS
Volume 11, Issue 1, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41467-020-17861-7
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Funding
- CHUSJRC
- Quebec government (MSSS)
- CHUSJ Foundation
- Canada Foundation for Innovation
- Canadian Institutes of Health Research (CIHR) [MOP-133711]
- Canada Foundation for Innovation (CFI) equipment grant Fonds des leaders [29970]
- Natural Sciences and Engineering Research Council of Canada (NSERC) [418113-2012 (NSERC PIN 392027)]
- GRSNC at Universite of Montreal
- Fonds de recherche du Quebec-Sante (FRQS)
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The structural organization of excitatory inputs supporting spike-timing-dependent plasticity (STDP) remains unknown. We performed a spine STDP protocol using two-photon (2P) glutamate uncaging (pre) paired with postsynaptic spikes (post) in layer 5 pyramidal neurons from juvenile mice. Here we report that pre-post pairings that trigger timing-dependent LTP (t-LTP) produce shrinkage of the activated spine neck and increase in synaptic strength; and post-pre pairings that trigger timing-dependent LTD (t-LTD) decrease synaptic strength without affecting spine shape. Furthermore, the induction of t-LTP with 2P glutamate uncaging in clustered spines (<5 mu m apart) enhances LTP through a NMDA receptor-mediated spine calcium accumulation and actin polymerization-dependent neck shrinkage, whereas t-LTD was dependent on NMDA receptors and disrupted by the activation of clustered spines but recovered when separated by >40 mu m. These results indicate that synaptic cooperativity disrupts t-LTD and extends the temporal window for the induction of t-LTP, leading to STDP only encompassing LTP.
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