Journal Article

DZNE-2021-00145

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png Loss of Ryanodine Receptor 2 impairs neuronal activity-dependent remodeling of dendritic spines and triggers compensatory neuronal hyperexcitability.

Bertan, F. (First author)DZNE* ; Wischhof, L.DZNE* ; Sosulina, L.DZNE* ; Mittag, M.DZNE* ; Dalügge, D.DZNE* ; Fornarelli, A.DZNE* ; Gardoni, F. ; Marcello, E. ; Di Luca, M. ; Fuhrmann, M.DZNE* ; Remy, S.DZNE* ; Bano, D. (Corresponding author)DZNE* ; Nicotera, P. (Last author)DZNE*

2020
Macmillan London

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Please use a persistent id in citations: doi:10.1038/s41418-020-0584-2

Abstract: Dendritic spines are postsynaptic domains that shape structural and functional properties of neurons. Upon neuronal activity, Ca2+ transients trigger signaling cascades that determine the plastic remodeling of dendritic spines, which modulate learning and memory. Here, we study in mice the role of the intracellular Ca2+ channel Ryanodine Receptor 2 (RyR2) in synaptic plasticity and memory formation. We demonstrate that loss of RyR2 in pyramidal neurons of the hippocampus impairs maintenance and activity-evoked structural plasticity of dendritic spines during memory acquisition. Furthermore, post-developmental deletion of RyR2 causes loss of excitatory synapses, dendritic sparsification, overcompensatory excitability, network hyperactivity and disruption of spatially tuned place cells. Altogether, our data underpin RyR2 as a link between spine remodeling, circuitry dysfunction and memory acquisition, which closely resemble pathological mechanisms observed in neurodegenerative disorders.

Keyword(s): Animals (MeSH) ; Dendritic Spines: physiology (MeSH) ; Female (MeSH) ; Hippocampus: metabolism (MeSH) ; Male (MeSH) ; Mice (MeSH) ; Mice, Inbred C57BL (MeSH) ; Mice, Knockout (MeSH) ; Neuronal Plasticity: physiology (MeSH) ; Pyramidal Cells: metabolism (MeSH) ; Ryanodine Receptor Calcium Release Channel: metabolism (MeSH) ; Synapses: physiology (MeSH)

Note: ISSN 1476-5403 not unique: **3 hits**.

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Contributing Institute(s):

1. Aging and neurodegeneration (AG Nicotera / Bano ; AG Bano)
2. Neuronal Networks (AG Remy)
3. Neuroimmunology and Imaging (AG Fuhrmann)

Research Program(s):

1. 341 - Molecular Signaling (POF3-341) (POF3-341)
2. 342 - Disease Mechanisms and Model Systems (POF3-342) (POF3-342)

Appears in the scientific report 2020

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Database coverage:
; ; ; BIOSIS Previews ; Biological Abstracts ; Clarivate Analytics Master Journal List ; Current Contents - Life Sciences ; Ebsco Academic Search ; Essential Science Indicators ; IF >= 10 ; JCR ; SCOPUS ; Science Citation Index Expanded ; Web of Science Core Collection

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Linked articles:

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png Journal Article (Erratum/Correction) Bertan, F. (First author)DZNE* ; Wischhof, L. (First author)DZNE* ; Sosulina, L. (First author)DZNE* ; Mittag, M. (First author)DZNE* ; Dalügge, D.DZNE* ; Fornarelli, A.DZNE* ; Gardoni, F. ; Marcello, E. ; Di Luca, M. ; Fuhrmann, M.DZNE* ; Remy, S.DZNE* ; Bano, D.DZNE* ; Nicotera, P. (Last author)DZNE*
Correction: Loss of Ryanodine Receptor 2 impairs neuronal activity-dependent remodeling of dendritic spines and triggers compensatory neuronal hyperexcitability.
Cell death and differentiation 28(3), 1134 - 1134 (2021) [10.1038/s41418-020-00605-x]2021   Files  Fulltext by Pubmed Central BibTeX | EndNote: XML, Text | RIS

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