Activation of glycogen synthase kinase-3 inhibits long-term potentiation with synapse-associated impairments
Open accessAbstract
Activation of glycogen synthase kinase-3 (GSK-3) can cause memory deficits as seen in Alzheimer's disease, the most common age-associated dementia, but the mechanism is not understood. Here, we found that activation of GSK-3 by wortmannin or transient overexpression of wild-type GSK-3β could suppress the induction of long-term potentiation (LTP) in rat hippocampus, whereas simultaneous inhibition of GSK-3 by lithium or SB216763 or transient expression of a dominant-negative GSK-3β mutant (dnGSK-3β) preserved the LTP. After high-frequency stimulation (HFS), the presynaptic release of glutamate and the expression/clustering of synapsin I, a synaptic vesicle protein playing an important role in neurotransmitter release, decreased markedly after upregulation of GSK-3.In vitro studies further demonstrated that GSK-3 inhibited the expression of SynI independent of HFS. In postsynaptic level, the expression of PSD93 and NR2A/B proteins decreased significantly when GSK-3 was activated. The LTP-associated synapse impairments including less presynaptic active zone, thinner postsynaptic density, and broader synaptic cleft were also prominent in the hippocampal slices after HFS with activation of GSK-3. These synaptic impairments were attenuated when GSK-3 was simultaneously inhibited by LiCl or SB216763 or transient expression of dnGSK-3. We conclude that upregulation of GSK-3 impairs the synaptic plasticity both functionally and structurally, which may underlie the GSK-3-involved memory deficits.
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GSK3β activation reduces synaptic long-term potentiation (LTP) and provides a potential biochemical mechanism by which Aβ can induce tau hyperphosphorylation.
“GSK3β activation reduces synaptic long-term potentiation (LTP) and provides a potential biochemical mechanism by which Aβ can induce τ hyperphosphorylation [39].”
From ApoE, ApoE Receptors, and the Synapse in Alzheimer's Disease (2017) · cites this paper as [39]
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- Authors
- Zhu, L.-Q., Wang, S.-H., Liu, D., Yin, Y.-Y., Tian, Q., Wang, X.-C., Wang, Q., Chen, J.-G., & Wang, J.-Z.
- Affiliations
- Huazhong University of Science and Technology (CN)
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2007-11-07
- Volume
- 27
- Issue
- 45
- Pages
- 12211-12220
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6673262
- OpenAlex
- W2045696000
- Cited by
- 234
- References
- 70
- Citations by year
- 2026: 4 · 2025: 6 · 2024: 2 · 2023: 9 · 2022: 9 · 2021: 13 · 2020: 11 · 2019: 6 · 2018: 16 · 2017: 10 · 2016: 17 · 2015: 18 · 2014: 25 · 2013: 19 · 2012: 18
- FWCI
- 4.25
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (30430270)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Keywords
- glycogen synthase kinase-3, GSK3β, long-term potentiation, synaptic plasticity, hippocampus, Alzheimer's disease, memory impairment, synapsin I, glutamate release, postsynaptic density, synaptic cleft, lithium, SB216763, wortmannin, high-frequency stimulation
- MeSH terms
- Animals, Enzyme Activation, Enzyme Inhibitors, Hippocampus, Male, Neural Inhibition, Synapses, Rats, Wistar, Long-Term Potentiation, Glycogen Synthase Kinase 3, Rats
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