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SynDIG4/Prrt1 Is Required for Excitatory Synapse Development and Plasticity Underlying Cognitive Function
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SynDIG4 slows deactivation kinetics of both GluA1 homomers and GluA1/GluA2 heteromers.
“Similar to other AMPAR auxiliary factors (Jackson and Nicoll, 2011), SynDIG4 slows deactivation kinetics of both GluA1 homomers and GluA1/GluA2 heteromers.”
From Loss of SynDIG4/PRRT1 alters distribution of AMPA receptors in Rab4- and Rab11-positive endosomes and impairs basal AMPA receptor recycling (2025) · cites this paper as Matt et al., 2018
Mice lacking SynDIG4 are impaired in single tetanus-induced LTP and NMDAR-dependent LTD.
“Mice lacking SynDIG4 have reduced surface expression of GluA1 and GluA2 and are impaired in single tetanus-induced long-term potentiation and NMDA receptor (NMDAR)-dependent long-term depression.”
From Loss of SynDIG4/PRRT1 alters distribution of AMPA receptors in Rab4- and Rab11-positive endosomes and impairs basal AMPA receptor recycling (2025) · cites this paper as Matt et al., 2018
Baseline synaptic transmission is intact in SynDIG4 KO neurons.
“Furthermore, NMDA receptor (NMDAR)-dependent long-term depression (LTD) (Troyano-Rodriguez et al., 2019) and single tetanus-induced long-term potentiation (LTP) (Matt et al., 2018) are impaired in SynDIG4 KO neurons while baseline synaptic transmission is intact.”
From Loss of SynDIG4/PRRT1 alters distribution of AMPA receptors in Rab4- and Rab11-positive endosomes and impairs basal AMPA receptor recycling (2025) · cites this paper as Matt et al., 2018
Total levels of AMPARs are unchanged in SynDIG4 KO mice.
“In SynDIG4 knockout (KO) mice, while total levels of AMPARs are unchanged, surface expression of GluA1 and GluA2 was significantly decreased (Troyano-Rodriguez et al., 2019).”
From Loss of SynDIG4/PRRT1 alters distribution of AMPA receptors in Rab4- and Rab11-positive endosomes and impairs basal AMPA receptor recycling (2025) · cites this paper as Matt et al., 2018
There is a significant decrease in extrasynaptic GluA1 and GluA2 in SynDIG4 KO neurons.
“Indeed, there is a significant decrease in extrasynaptic GluA1 and GluA2 in SynDIG4 KO neurons (Matt et al., 2018).”
From Loss of SynDIG4/PRRT1 alters distribution of AMPA receptors in Rab4- and Rab11-positive endosomes and impairs basal AMPA receptor recycling (2025) · cites this paper as Matt et al., 2018
Both NMDAR-dependent LTD and single tetanus-induced LTP are impaired in SynDIG4 deficient neurons while baseline synaptic transmission is intact.
“Intriguingly, both NMDAR-dependent LTD (Troyano-Rodriguez et al., 2019) and single tetanus-induced LTP (Matt et al., 2018), which require calcium-permeable AMPARs (Sanderson et al., 2016), which are mostly GluA1 homomers, are impaired in SynDIG4 deficient neurons while baseline synaptic transmission is intact.”
From Loss of SynDIG4/PRRT1 alters distribution of AMPA receptors in Rab4- and Rab11-positive endosomes and impairs basal AMPA receptor recycling (2025) · cites this paper as Matt et al., 2018
Previous work showed reduced density of extrasynaptic GluA1 and GluA2 puncta in SynDIG4 KO neurons.
“Previous work showed decreased surface expression of GluA1 and GluA2 (Troyano-Rodriguez et al., 2019) and reduced density of extrasynaptic GluA1 and GluA2 puncta in SynDIG4 KO neurons (Matt et al., 2018).”
From Loss of SynDIG4/PRRT1 alters distribution of AMPA receptors in Rab4- and Rab11-positive endosomes and impairs basal AMPA receptor recycling (2025) · cites this paper as Matt et al., 2018
In Xenopus oocytes, SynDIG4 modulates AMPAR gating properties in a subunit-dependent manner.
“In Xenopus oocytes, SynDIG4 was shown to modulate AMPAR gating properties in a subunit-dependent manner (Matt et al., 2018).”
From Loss of SynDIG4/PRRT1 alters distribution of AMPA receptors in Rab4- and Rab11-positive endosomes and impairs basal AMPA receptor recycling (2025) · cites this paper as Matt et al., 2018
SynDIG4 KO neurons display deficits in LTD and single-tetanus LTP, both of which require GluA1.
“SynDIG4 KO neurons display deficits in LTD (Troyano-Rodriguez et al., 2019) and single-tetanus LTP (Matt et al., 2018), both of which require GluA1.”
From Loss of SynDIG4/PRRT1 alters distribution of AMPA receptors in Rab4- and Rab11-positive endosomes and impairs basal AMPA receptor recycling (2025) · cites this paper as Matt et al., 2018
SynDIG4 KO mice display deficits in hippocampal-dependent learning and memory.
“SynDIG4 KO mice also display deficits in hippocampal-dependent learning and memory (Matt et al., 2018), and downregulation of SynDIG4 has been found in patients with Alzheimer’s disease (Li et al., 2021).”
From Loss of SynDIG4/PRRT1 alters distribution of AMPA receptors in Rab4- and Rab11-positive endosomes and impairs basal AMPA receptor recycling (2025) · cites this paper as Matt et al., 2018
SynDIG4 reduces desensitization only of GluA1 homomers and has no significant effect on desensitization of heteromeric GluA1/GluA2.
“In contrast, SynDIG4 reduces desensitization only of GluA1 homomers and has no significant effect on desensitization of heteromeric GluA1/GluA2 (Matt et al., 2018).”
From Loss of SynDIG4/PRRT1 alters distribution of AMPA receptors in Rab4- and Rab11-positive endosomes and impairs basal AMPA receptor recycling (2025) · cites this paper as Matt et al., 2018
There is a reduction in sGluA1-containing AMPARs at or near PSD95 in SynDIG4 KO neurons.
“These findings suggest a reduction in sGluA1-containing AMPARs at or near PSD95, consistent with the observed decrease in miniature excitatory postsynaptic current (mEPSC) amplitude in SynDIG4 KO mice (Matt et al., 2018).”
From Loss of SynDIG4/PRRT1 alters distribution of AMPA receptors in Rab4- and Rab11-positive endosomes and impairs basal AMPA receptor recycling (2025) · cites this paper as Matt et al., 2018
SynDIG4 functions as an auxiliary factor of AMPARs and plays a critical role in excitatory synaptic plasticity and hippocampal-dependent learning and memory.
“The transmembrane protein Synapse Differentiation Induced Gene 4 (SynDIG4) functions as an auxiliary factor of AMPA receptors (AMPARs) and plays a critical role in excitatory synaptic plasticity as well as hippocampal-dependent learning and memory.”
From Loss of SynDIG4/PRRT1 alters distribution of AMPA receptors in Rab4- and Rab11-positive endosomes and impairs basal AMPA receptor recycling (2025) · cites this paper as Matt et al., 2018
Under confocal microscopy, the density of GluA1 puncta was increased in synaptic regions identified by overlap with the presynaptic marker vGLUT1 in SynDIG4 KO mice.
“Interestingly, under confocal microscopy, the density of GluA1 puncta was increased in synaptic regions identified by overlap with the presynaptic marker vGLUT1 (Matt et al., 2018).”
From Loss of SynDIG4/PRRT1 alters distribution of AMPA receptors in Rab4- and Rab11-positive endosomes and impairs basal AMPA receptor recycling (2025) · cites this paper as Matt et al., 2018
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Citations
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Sorted by citations
Structure, Function, and Pharmacology of Glutamate Receptor Ion Channels
Hansen, K. B., Wollmuth, L. P., Bowie, D., Furukawa, H., Menniti, F. S., Sobolevsky, A. I., Swanson, G. T., Swanger, S. A., Greger, I. H., Nakagawa, T., et al. (2021) · Pharmacological Reviews · doi:10.1124/pharmrev.120.000131 · Cited by 686
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Metadata
- Authors
- Matt, L., Kirk, L. M., Chenaux, G., Speca, D. J., Puhger, K. R., Pride, M. C., Qneibi, M., Haham, T., Plambeck, K. E., Stern-Bach, Y., Silverman, J. L., Crawley, J. N., Hell, J. W., & Díaz, E.
- Venue
- Cell Reports
- Publisher
- Elsevier BV
- Published
- 2018-02
- Volume
- 22
- Issue
- 9
- Pages
- 2246-2253
- ISSN
- 2211-1247
- PMC
- PMC5856126
- Cited by
- 73
- References
- 5
- Language
- en
- Licence
- Funders
- Whitehall Foundation (2015-05-106)
- American Heart Association (11POST7020009)
- United States-Israel Binational Science Foundation
- National Science Foundation (1322302)
- Bloom's Syndrome Foundation (2012781)
- National Institutes of Health (U54 HD079125 MCP, R01 MH097887, DP2 OD006479-01, R01 NS078792)
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