ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014
Phosphorylation of synapsin I by cyclin-dependent kinase-5 sets the ratio between the resting and recycling pools of synaptic vesicles at hippocampal synapses.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 83 citations in OpenAlex.
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- An unsuspected physiological role for mGluRIII glutamate receptors in hippocampal area CA1.Cell reports · 2026Article
- An electrophysiological and proteomics roadmap for human induced glutamatergic neurons: fine-tuning of culture conditions for pathophysiological studies.Cell death discovery · 2026Article
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- Memory Decline and Aberration of Synaptic Proteins in X-Linked Moesin Knockout Male Mice.Psychiatry investigation · 2025Article
- Hydroxynorketamine, but not ketamine, acts via α7 nicotinic acetylcholine receptor to control presynaptic function and gene expression.Translational psychiatry · 2024Article
- Orchestrating vesicular and nonvesicular membrane dynamics by intrinsically disordered proteins.EMBO reports · 2023Review
- The Neurotoxic Effect of Environmental Temperature Variation in Adult Zebrafish (International journal of molecular sciences · 2023Article
- Adaptor protein AP-3 produces synaptic vesicles that release at high frequency by recruiting phospholipid flippase ATP8A1.Nature neuroscience · 2023Article
- miR-329- and miR-495-mediated Prr7 down-regulation is required for homeostatic synaptic depression in rat hippocampal neurons.Life science alliance · 2022Article
- Bassoon controls synaptic vesicle release via regulation of presynaptic phosphorylation and cAMP.EMBO reports · 2022Article
- Downregulation of CDK5 signaling in the dorsal striatum alters striatal microcircuits implicating the association of pathologies with circadian behavior in mice.Molecular brain · 2022Article
- Low p-SYN1 (Ser-553) Expression Leads to Abnormal Neurotransmitter Release of GABA Induced by Up-Regulated Cdk5 after Microwave Exposure: Insights on Protection and Treatment of Microwave-Induced Cognitive Dysfunction.Current issues in molecular biology · 2021Article
- Aβ1-16 controls synaptic vesicle pools at excitatory synapses via cholinergic modulation of synapsin phosphorylation.Cellular and molecular life sciences : CMLS · 2021Article
- Molecular Mechanisms of Memory Consolidation That Operate During Sleep.Frontiers in molecular neuroscience · 2021Review
- A comparative analysis of the mobility of 45 proteins in the synaptic bouton.The EMBO journal · 2020Article
- Cystatin C promotes cognitive dysfunction in rats with cerebral microbleeds by inhibiting the ERK/synapsin Ia/Ib pathway.Experimental and therapeutic medicine · 2020Article
- Changes in Synaptic Proteins Precede Neurodegeneration Markers in Preclinical Alzheimer's Disease Cerebrospinal Fluid.Molecular & cellular proteomics : MCP · 2019Article
- Overexpression of miR-1 in the heart attenuates hippocampal synaptic vesicle exocytosis by the posttranscriptional regulation of SNAP-25 through the transportation of exosomes.Cell communication and signaling : CCS · 2018Article
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
Cyclin-dependent kinase-5 (Cdk5) was reported to downscale neurotransmission by sequestering synaptic vesicles (SVs) in the release-reluctant resting pool, but the molecular targets mediating this activity remain unknown. Synapsin I (SynI), a major SV phosphoprotein involved in the regulation of SV trafficking and neurotransmitter release, is one of the presynaptic substrates of Cdk5, which phosphorylates it in its C-terminal region at Ser(549) (site 6) and Ser(551) (site 7). Here we demonstrate that Cdk5 phosphorylation of SynI fine tunes the recruitment of SVs to the active recycling pool and contributes to the Cdk5-mediated homeostatic responses. Phosphorylation of SynI by Cdk5 is physiologically regulated and enhances its binding to F-actin. The effects of Cdk5 inhibition on the size and depletion kinetics of the recycling pool, as well as on SV distribution within the nerve terminal, are virtually abolished in mouse SynI knock-out (KO) neurons or in KO neurons expressing the dephosphomimetic SynI mutants at sites 6,7 or site 7 only. The observation that the single site-7 mutant phenocopies the effects of the deletion of SynI identifies this site as the central switch in mediating the synaptic effects of Cdk5 and demonstrates that SynI is necessary and sufficient for achieving the effects of the kinase on SV trafficking. The phosphorylation state of SynI by Cdk5 at site 7 is regulated during chronic modification of neuronal activity and is an essential downstream effector for the Cdk5-mediated homeostatic scaling.
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