The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.
MicroRNA regulation of homeostatic synaptic plasticity
Abstract
Homeostatic mechanisms are required to control formation and maintenance of synaptic connections to maintain the general level of neural impulse activity within normal limits. How genes controlling these processes are co-coordinately regulated during homeostatic synaptic plasticity is unknown. MicroRNAs (miRNAs) exert regulatory control over mRNA stability and translation and may contribute to local and activity-dependent posttranscriptional control of synapse-associated mRNAs. However, identifying miRNAs that function through posttranscriptional gene silencing at synapses has remained elusive. Using a bioinformatics screen to identify sequence motifs enriched in the 3′UTR of rapidly destabilized mRNAs, we identified a developmentally and activity-regulated miRNA (miR-485) that controls dendritic spine number and synapse formation in an activity-dependent homeostatic manner. We find that many plasticity-associated genes contain predicted miR-485 binding sites and further identify the presynaptic protein SV2A as a target of miR-485. miR-485 negatively regulated dendritic spine density, postsynaptic density 95 (PSD-95) clustering, and surface expression of GluR2. Furthermore, miR-485 overexpression reduced spontaneous synaptic responses and transmitter release, as measured by miniature excitatory postsynaptic current (EPSC) analysis and FM 1–43 staining. SV2A knockdown mimicked the effects of miR-485, and these effects were reversed by SV2A overexpression. Moreover, 5 d of increased synaptic activity induced homeostatic changes in synaptic specializations that were blocked by a miR-485 inhibitor. Our findings reveal a role for this previously uncharacterized miRNA and the presynaptic protein SV2A in homeostatic plasticity and nervous system development, with possible implications in neurological disorders (e.g., Huntington and Alzheimer's disease), where miR-485 has been found to be dysregulated.
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“Notably, significantly enriched motifs among these lesser abundant seeds include those corresponding to miRNAs previously described as brain-enriched (e.g., miR-101, miR-153, and miR-485) or having synaptic (e.g., miR-138) or glial (e.g., miR-23) localization (Cohen et al., 2011; Farh et al., 2005; Lagos-Quintana et al., 2002; Sempere et al., 2004; Siegel et al., 2009; Smirnova et al., 2005), sign”
From Transcriptome-wide Discovery of microRNA Binding Sites in Human Brain (2014) · cites this paper as Cohen et al., 2011
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“This notion is further supported by data in hippocampal cultures, where miR‐485 regulates levels of specific pre‐ and postsynaptic proteins (Cohen et al., 2011)”
From MicroRNA‐138‐5p suppresses excitatory synaptic strength at the cerebellar input layer (2025) · cites this paper as Cohen et al., 2011
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Metadata
- Authors
- Cohen, J. E., Lee, P. R., Chen, S., Li, W., & Fields, R. D.
- Affiliations
- Section on Nervous System Development and Plasticity, The Eunice Kennedy Shriver National Institute of Child and Human Development, National Institutes of Health, Bethesda, MD 20892-3714; and
- Unit on Retinal Neurophysiology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892-2510
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2011-06-22
- Volume
- 108
- Issue
- 28
- Pages
- 11650-11655
- ISSN
- 0027-8424
- 1091-6490
- Cited by
- 202
- References
- 11
- Language
- en
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