Synaptopodin regulates denervation-induced plasticity at hippocampal mossy fiber synapses
Abstract: Neurological diseases can lead to the denervation of brain regions caused by demyelination, traumatic injury or cell death. The molecular and structural mechanisms underlying lesion-induced reorganization of denervated brain regions, however, are a matter of ongoing investigation. In order to address this issue, we performed an entorhinal cortex lesion (ECL) in mouse organotypic entorhino-hippocampal tissue cultures of both sexes and studied denervation-induced plasticity of mossy fiber synapses, which connect dentate granule cells (dGCs) with CA3 pyramidal cells (CA3-PCs) and play important roles in learning and memory formation. Partial denervation caused a strengthening of excitatory neurotransmission in dGCs, CA3-PCs and their direct synaptic connections, as revealed by paired recordings (dGC-to-CA3-PC). These functional changes were accompanied by ultrastructural reorganization of mossy fiber synapses, which regularly contain the plasticity-regulating protein synaptopodin and the spine apparatus organelle. We demonstrate that the spine apparatus organelle and synaptopodin are related to ribosomes in close proximity to synaptic sites and reveal a synaptopodin-related transcriptome. Notably, synaptopodin-deficient tissue preparations that lack the spine apparatus organelle failed to express lesion-induced synaptic adjustments. Hence, synaptopodin and the spine apparatus organelle play a crucial role in regulating lesion-induced synaptic plasticity at hippocampal mossy fiber synapses
- Standort
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Deutsche Nationalbibliothek Frankfurt am Main
- Umfang
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Online-Ressource
- Sprache
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Englisch
- Anmerkungen
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Cells. - 13, 2 (2024) , 114, ISSN: 2073-4409
- Ereignis
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Veröffentlichung
- (wo)
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Freiburg
- (wer)
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Universität
- (wann)
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2024
- Urheber
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Kruse, Pia
Brandes, Gudrun
Hemeling, Hanna
Huang, Zhong
Wrede, Christoph
Hegermann, Jan
Vlachos, Andreas
Lenz, Maximilian Christopher
- DOI
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10.3390/cells13020114
- URN
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urn:nbn:de:bsz:25-freidok-2433819
- Rechteinformation
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Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Letzte Aktualisierung
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25.03.2025, 13:49 MEZ
Datenpartner
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Beteiligte
- Kruse, Pia
- Brandes, Gudrun
- Hemeling, Hanna
- Huang, Zhong
- Wrede, Christoph
- Hegermann, Jan
- Vlachos, Andreas
- Lenz, Maximilian Christopher
- Universität
Entstanden
- 2024