Cited by 17Neuroscience and Neuropharmacology ResearchCellular transport and secretionMemory and Neural Mechanisms

Syntaxin-3 is dispensable for basal neurotransmission and synaptic plasticity in postsynaptic hippocampal CA1 neurons

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Shi, Shan, Ma, Ke, Bin, Na-Ryum, Harada, Hidekiyo, Xie, Xiaoyu, Huang, Mengjia, Liu, Haiyu, Lee, Soomin +5 more·2020·Scientific Reports

Abstract

Recent evidence suggests that SNARE fusion machinery play critical roles in postsynaptic neurotransmitter receptor trafficking, which is essential for synaptic plasticity. However, the key SNAREs involved remain highly controversial; syntaxin-3 and syntaxin-4 are leading candidates for the syntaxin isoform underlying postsynaptic plasticity. In a previous study, we showed that pyramidal-neuron specific conditional knockout (cKO) of syntaxin-4 significantly reduces basal transmission, synaptic plasticity and impairs postsynaptic receptor trafficking. However, this does not exclude a role for syntaxin-3 in such processes. Here, we generated and analyzed syntaxin-3 cKO mice. Extracellular field recordings in hippocampal slices showed that syntaxin-3 cKO did not exhibit significant changes in CA1 basal neurotransmission or in paired-pulse ratios. Importantly, there were no observed differences during LTP in comparison to control mice. Syntaxin-3 cKO mice performed similarly as the controls in spatial and contextual learning tasks. Consistent with the minimal effects of syntaxin-3 cKO, syntaxin-3 mRNA level was very low in hippocampal and cortex pyramidal neurons, but strongly expressed in the corpus callosum and caudate axon fibers. Together, our data suggest that syntaxin-3 is dispensable for hippocampal basal neurotransmission and synaptic plasticity, and further supports the notion that syntaxin-4 is the major isoform mediating these processes.

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  • Stx-3 is reported to be required for LTP.

    “On the one hand Stx-3 is reported to be required for LTP (Ref. 334, but see Ref. 339)”

    From Synaptic memory and CaMKII (2023) · cites this paper as [339]

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Authors
Shi, S., Ma, K., Bin, N.-R., Harada, H., Xie, X., Huang, M., Liu, H., Lee, S., Wang, X. F., Adachi, R., Monnier, P. P., Zhang, L., & Sugita, S.
Affiliations
  • University Health Network (CA)
  • The University of Texas MD Anderson Cancer Center (US)
Corresponding author
  • Ma, Ke
  • Sugita, Shuzo
Venue
Scientific Reports
Published
2020-01-20
Volume
10
Issue
1
Pages
709-709
ISSN
2045-2322 (ISSN-L)
OpenAlex
W3002680483
Cited by
17
References
0
Citations by year
2026: 2 · 2025: 3 · 2024: 4 · 2023: 4 · 2022: 2 · 2021: 2
FWCI
0.92
Type
journal article
Language
en
Open access
Locations
  • Scientific Reports (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
Funders
  • Canadian Network for Research and Innovation in Machining Technology, Natural Sciences and Engineering Research Council of Canada (CGS-D2, 06438)
  • Gouvernement du Canada | Canadian Institutes of Health Research (93665, 130573)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular transport and secretion
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
Keywords
syntaxin 3, syntaxin 4, SNARE proteins, synaptic vesicle fusion, synaptic plasticity, long-term potentiation, CA1 pyramidal neurons, conditional knockout mice, paired-pulse ratio, spatial learning, contextual learning, corpus callosum
MeSH terms
Animals, Corpus Callosum, Synaptic Transmission, Neuronal Plasticity, RNA, Messenger, Gene Expression, Long-Term Potentiation, Mice, Knockout, Qa-SNARE Proteins, CA1 Region, Hippocampal, In Vitro Techniques

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