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Impairment of L-type Ca2+Channel-Dependent Forms of Hippocampal Synaptic Plasticity in Mice Deficient in the Extracellular Matrix Glycoprotein Tenascin-C
Open accessAbstract
The extracellular matrix glycoprotein tenascin-C (TN-C) has been suggested to play important functional roles during neural development, axonal regeneration, and synaptic plasticity. We generated a constitutively TN-C-deficient mouse mutant from embryonic stem cells with a floxed tn-C allele, representing a standard for future analysis of conditionally targeted mice. The gross morphology of the CNS was not detectably affected, including no evidence for perturbed nerve cell migration, abnormal oligodendrocyte distribution, or defective myelination. Despite the apparent normal histology of the hippocampus and normal performance in the water maze, theta-burst stimulation (TBS) of Schaffer collaterals elicited reduced long-term potentiation (LTP) in the CA1 region of TN-C-deficient mutants, as compared with wild-type littermates. However, high-frequency stimulation evoked normal LTP not only in CA1, but also at mossy fiber-CA3 and medial and lateral perforant path-granule cell synapses in the dentate gyrus. Low-frequency stimulation failed to induce long-term depression in the CA1 region of TN-C-deficient animals. Recordings of TBS-induced LTP in the presence of nifedipine, an antagonist of L-type voltage-dependent Ca2+ channels (VDCCs), did not affect LTP in TN-C-deficient mice, but reduced LTP in wild-type mice to the levels seen in mutants. Furthermore, chemical induction of a L-type VDCC-dependent LTP in the CA1 region by application of the K+ channel blocker tetraethylammonium resulted in impaired LTP in TN-C mutants. Thus, reduction in L-type VDCC-mediated signaling appears to mediate the deficits in certain forms of synaptic plasticity in constitutively TN-C-deficient mice.
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“Lastly, animals deficient in tenascin-C show impaired L-type calcium channel-dependent LTP [74].”
From The extracellular matrix and perineuronal nets in memory (2022) · cites this paper as [74]
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“When the composition of PNNs is impaired, the neuronal synaptic plasticity in form of LTP is affected, as has been reported for the tenascin-C (TnC)7, TnR25, brevican26 and neurocan27 knockout mice.”
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Metadata
- Authors
- Evers, M. R., Salmen, B., Bukalo, O., Rollenhagen, A., Bösl, M. R., Morellini, F., Bartsch, U., Dityatev, A., & Schachner, M.
- Affiliations
- Universität Hamburg (DE)
- ORCID
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2002-08-15
- Volume
- 22
- Issue
- 16
- Pages
- 7177-7194
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6757873
- OpenAlex
- W2141616957
- Cited by
- 172
- References
- 81
- Citations by year
- 2026: 4 · 2025: 6 · 2024: 5 · 2023: 5 · 2022: 9 · 2021: 8 · 2020: 3 · 2019: 3 · 2018: 9 · 2017: 7 · 2016: 7 · 2015: 4 · 2014: 9 · 2013: 6 · 2012: 10
- FWCI
- 3.38
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Neuroscience (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Rutgers University Community Repository (Rutgers University) (submittedVersion)
- Funders
- Deutsche Forschungsgemeinschaft
- Rheinische Friedrich-Wilhelms-Universität Bonn
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Keywords
- tenascin-C, extracellular matrix, L-type calcium channels, hippocampal synaptic plasticity, long-term potentiation, long-term depression, CA1 region, dentate gyrus, Schaffer collaterals, perforant path, tetraethylammonium, nifedipine, floxed allele
- MeSH terms
- Animals, Behavior, Animal, Cerebellar Cortex, Electric Stimulation, Hippocampus, Male, Neural Inhibition, Neuronal Plasticity, Neurons, Optic Nerve, Retina, Synapses, Blotting, Western, Long-Term Potentiation, Mice, Knockout, Gene Targeting, Excitatory Amino Acid Antagonists, Maze Learning, Tenascin, Excitatory Postsynaptic Potentials, Calcium Channels, L-Type, Mice, In Vitro Techniques
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