Journal
CELL REPORTS
Volume 25, Issue 13, Pages 3631-+Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2018.12.010
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Funding
- World-Class University (WCU) program through the National Research Foundation of Korea [R32-10142]
- National Research Foundation of Korea (NRF) - Korean government (Ministry of Science, ICT and Future Planning [MSIP]) [2018R1A5A2025964]
- U.K. Medical Research Council (MRC) [MR/K023098/1]
- Biotechnology and Biological Sciences Research Council (BBSRC) [BB/K019899/1]
- European Union (EU) [341089-HippoKAR]
- Canadian Institutes of Health Research (CIHR) Foundation [154276]
- Brain Canada Foundation through the Canada Brain Research Fund
- Health Canada
- BBSRC [BB/K019899/1] Funding Source: UKRI
- MRC [MR/K023098/1] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/K019899/1] Funding Source: researchfish
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A major mechanism contributing to synaptic plasticity involves alterations in the number of AMPA receptors (AMPARs) expressed at synapses. Hippo-campal CA1 synapses, where this process has been most extensively studied, are highly heterogeneous with respect to their probability of neurotransmitter release, P(r). It is unknown whether there is any relationship between the extent of plasticity-related AMPAR trafficking and the initial P(r) of a synapse. To address this question, we induced metabotropic glutamate receptor (mGluR) dependent long-term depression (mGluR-LTD) and assessed AMPAR trafficking and P(r) at individual synapses, using SEPGluA2 and FM4-64, respectively. We found that either pharmacological or synaptic activation of mGluR1 reduced synaptic SEP-GluA2 in a manner that depends upon P(r); this process involved an activity-dependent reduction in surface mGluR1 that selectively protects high-P(r) synapses from synaptic weakening. Consequently, the extent of postsynaptic plasticity can be pre-tuned by presynaptic activity.
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