%0 Journal Article
%A Bertan, Fabio
%A Wischhof, Lena
%A Sosulina, Liudmila
%A Mittag, Manuel
%A Dalügge, Dennis
%A Fornarelli, Alessandra
%A Gardoni, Fabrizio
%A Marcello, Elena
%A Di Luca, Monica
%A Fuhrmann, Martin
%A Remy, Stefan
%A Bano, Daniele
%A Nicotera, Pierluigi
%T Loss of Ryanodine Receptor 2 impairs neuronal activity-dependent remodeling of dendritic spines and triggers compensatory neuronal hyperexcitability.
%J Cell death and differentiation
%V 27
%N 12
%@ 1476-5403
%C London
%I Macmillan
%M DZNE-2021-00145
%P 3354 - 3373
%D 2020
%Z ISSN 1476-5403 not unique: **3 hits**.
%X 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.
%K Animals
%K Dendritic Spines: physiology
%K Female
%K Hippocampus: metabolism
%K Male
%K Mice
%K Mice, Inbred C57BL
%K Mice, Knockout
%K Neuronal Plasticity: physiology
%K Pyramidal Cells: metabolism
%K Ryanodine Receptor Calcium Release Channel: metabolism
%K Synapses: physiology
%F PUB:(DE-HGF)16
%9 Journal Article
%$ pmid:32641776
%2 pmc:PMC7853040
%R 10.1038/s41418-020-0584-2
%U https://pub.dzne.de/record/154291