The role of SAP97 in synaptic glutamate receptor dynamics
Abstract
Proteins of the PSD-95–like membrane-associated guanylate kinase (PSD-MAGUK) family are vital for trafficking AMPA receptors (AMPARs) to synapses, a process necessary for both basal synaptic transmission and forms of synaptic plasticity. Synapse-associated protein 97 (SAP97) exhibits protein interactions, such as direct interaction with the GluA1 AMPAR subunit, and subcellular localization (synaptic, perisynaptic, and dendritic) unique within this protein family. Due in part to the lethality of the germline knockout of SAP97, this protein’s role in synaptic transmission and plasticity is poorly understood. We found that overexpression of SAP97 during early development traffics AMPARs and NMDA receptors (NMDARs) to synapses, and that SAP97 rescues the deficits in AMPAR currents normally seen in PSD-93/-95 double-knockout neurons. Mature neurons that have experienced the overexpression of SAP97 throughout development exhibit enhanced AMPAR and NMDAR currents, as well as faster NMDAR current decay kinetics. In loss-of-function experiments using conditional SAP97 gene deletion, we recorded no deficits in glutamatergic transmission or long-term potentiation. These results support the hypothesis that SAP97 is part of the machinery that traffics glutamate receptors and compensates for other PSD-MAGUKs in knockout mouse models. However, due to functional redundancy, other PSD-MAGUKs can presumably compensate when SAP97 is conditionally deleted during development.
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The effects of SAP97 overexpression on synaptic transmission are influenced by isoforms of SAP97, compensation with other PSD-MAGUKs, or matureness of synapse.
“The effects of SAP97 overexpression on synaptic transmission seem to be influenced by many factors, such as isoforms of SAP97 (Schlu ¨ter et al., 2006;Waites et al., 2009), compensation with other PSD-MAGUKs (Schlu ¨ter et al., 2006;Howard et al., 2010), or matureness of synapse (Howard et al., 2010).”
From The Brain-Enriched MicroRNA miR-9-3p Regulates Synaptic Plasticity and Memory (2016) · cites this paper as Howard et al., 2010
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Cites
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Self-citationStargazin regulates synaptic targeting of AMPA receptors by two distinct mechanisms
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Self-citationRegulation of AMPA receptor trafficking and synaptic plasticity
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“Indeed, over-expression of either SAP97 or SAP102 fully restores glutamatergic transmission in neurons derived from PSD-93/PSD-95 double-knockout mice (Elias et al., 2006; Howard et al., 2010).”
BackgroundThe Brain-Enriched MicroRNA miR-9-3p Regulates Synaptic Plasticity and Memory
Sim, S.-E., Lim, C.-S., Kim, J.-I., Seo, D., Chun, H., Yu, N.-K., Lee, J., Kang, S. J., Ko, H.-G., Choi, J.-H., et al. (2016) · The Journal of Neuroscience · doi:10.1523/jneurosci.0630-16.2016 · Cited by 116 · see citing works
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Scribble1/AP2 complex coordinates NMDA receptor endocytic recycling
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- Authors
- Howard, M. A., Elias, G. M., Elias, L. A. B., Swat, W., & Nicoll, R. A.
- Affiliations
- Department of Cellular and Molecular Pharmacology,
- Neuroscience Graduate Program and Institute of Regenerative Medicine, University of California, San Francisco, CA 94143; and
- Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2010-02-23
- Volume
- 107
- Issue
- 8
- Pages
- 3805-3810
- ISSN
- 0027-8424
- 1091-6490
- Cited by
- 119
- References
- 3
- Language
- en
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