Loss of Ryanodine Receptor 2 impairs neuronal activity-dependent remodeling of dendritic spines and triggers compensatory neuronal hyperexcitability
Articolo
Data di Pubblicazione:
2020
Citazione:
Loss of Ryanodine Receptor 2 impairs neuronal activity-dependent remodeling of dendritic spines and triggers compensatory neuronal hyperexcitability / F. Bertan, L. Wischhof, L. Sosulina, M. Mittag, D. Dalugge, A. Fornarelli, F. Gardoni, E. Marcello, M. Di Luca, M. Fuhrmann, S. Remy, D. Bano, P. Nicotera. - In: CELL DEATH AND DIFFERENTIATION. - ISSN 1350-9047. - 27:(2020 Dec), pp. 3354-3373. [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.
Tipologia IRIS:
01 - Articolo su periodico
Elenco autori:
F. Bertan, L. Wischhof, L. Sosulina, M. Mittag, D. Dalugge, A. Fornarelli, F. Gardoni, E. Marcello, M. Di Luca, M. Fuhrmann, S. Remy, D. Bano, P. Nicotera
Link alla scheda completa:
Link al Full Text: