Journal
CELL REPORTS
Volume 22, Issue 9, Pages 2246-2253Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2018.02.026
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Funding
- American Heart Association [11POST7020009]
- Brain & Behavior Research Foundation NARSAD Young Investigator [20748]
- United States-Israel Binational Science Foundation (BSF) [2012781]
- United States National Science Foundation (NSF) [1322302]
- NIH [R01 MH097887, R01 NS078792, U54 HD079125]
- NIH New Director's Innovator Award Program [DP2 OD006479-01]
- UC Davis Academic Senate Research Program Pilot Grant
- Whitehall Foundation [2015-05-106]
- UC Davis MCB T32 Training Program [GM007377]
- Direct For Biological Sciences [1322302] Funding Source: National Science Foundation
- Division Of Integrative Organismal Systems [1322302] Funding Source: National Science Foundation
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Altering AMPA receptor (AMPAR) content at synapses is a key mechanism underlying the regulation of synaptic strength during learning and memory. Previous work demonstrated that SynDIG1 (synapse differentiation-induced gene 1) encodes a transmembrane AMPAR-associated protein that regulates excitatory synapse strength and number. Here we show that the related protein SynDIG4 (also known as Prrt1) modifies AMPAR gating properties in a subunit-dependent manner. Young SynDIG4 knockout (KO) mice have weaker excitatory synapses, as evaluated by immunocytochemistry and electrophysiology. Adult SynDIG4 KO mice show complete loss of tetanus-induced long-term potentiation (LTP), while mEPSC amplitude is reduced by only 25%. Furthermore, SynDIG4 KO mice exhibit deficits in two independent cognitive assays. Given that SynDIG4 colocalizes with the AMPAR subunit GluA1 at non-synaptic sites, we propose that SynDIG4 maintains a pool of extrasynaptic AMPARs necessary for synapse development and function underlying higher-order cognitive plasticity.
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