| First Author | Bertan F | Year | 2020 |
| Journal | Cell Death Differ | Volume | 27 |
| Issue | 12 | Pages | 3354-3373 |
| PubMed ID | 32641776 | Mgi Jnum | J:302783 |
| Mgi Id | MGI:6510154 | Doi | 10.1038/s41418-020-0584-2 |
| Citation | Bertan F, et al. (2020) Loss of Ryanodine Receptor 2 impairs neuronal activity-dependent remodeling of dendritic spines and triggers compensatory neuronal hyperexcitability. Cell Death Differ 27(12):3354-3373 |
| abstractText | Dendritic spines are postsynaptic domains that shape structural and functional properties of neurons. Upon neuronal activity, Ca(2+) 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 Ca(2+) 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. |
