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Article

Calsequestrin Deletion Facilitates Hippocampal Synaptic Plasticity and Spatial Learning in Post-Natal Development

1
Department of Biomolecular Sciences, Università di Urbino Carlo Bo, I-61029 Urbino, Italy
2
Department of Experimental and Clinical Medicine, Faculty of Medicine and Surgery, Università Politecnica delle Marche, I-60121 Ancona, Italy
3
Center for Advanced Studies and Technology & Department of Medicine and Aging Sciences, Università G. d’Annunzio, I-66100 Chieti, Italy
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2020, 21(15), 5473; https://doi.org/10.3390/ijms21155473
Received: 5 June 2020 / Revised: 15 July 2020 / Accepted: 30 July 2020 / Published: 31 July 2020
(This article belongs to the Special Issue Molecular Mechanisms of Neural Circuit Development and Regeneration)
Experimental evidence highlights the involvement of the endoplasmic reticulum (ER)-mediated Ca2+ signals in modulating synaptic plasticity and spatial memory formation in the hippocampus. Ca2+ release from the ER mainly occurs through two classes of Ca2+ channels, inositol 1,4,5-trisphosphate receptors (InsP3Rs) and ryanodine receptors (RyRs). Calsequestrin (CASQ) and calreticulin (CR) are the most abundant Ca2+-binding proteins allowing ER Ca2+ storage. The hippocampus is one of the brain regions expressing CASQ, but its role in neuronal activity, plasticity, and the learning processes is poorly investigated. Here, we used knockout mice lacking both CASQ type-1 and type-2 isoforms (double (d)CASQ-null mice) to: a) evaluate in adulthood the neuronal electrophysiological properties and synaptic plasticity in the hippocampal Cornu Ammonis 1 (CA1) field and b) study the performance of knockout mice in spatial learning tasks. The ablation of CASQ increased the CA1 neuron excitability and improved the long-term potentiation (LTP) maintenance. Consistently, (d)CASQ-null mice performed significantly better than controls in the Morris Water Maze task, needing a shorter time to develop a spatial preference for the goal. The Ca2+ handling analysis in CA1 pyramidal cells showed a decrement of Ca2+ transient amplitude in (d)CASQ-null mouse neurons, which is consistent with a decrease in afterhyperpolarization improving LTP. Altogether, our findings suggest that CASQ deletion affects activity-dependent ER Ca2+ release, thus facilitating synaptic plasticity and spatial learning in post-natal development. View Full-Text
Keywords: calcium dynamics; cognitive functions; neural plasticity; hippocampus; pyramidal neurons; adult mouse calcium dynamics; cognitive functions; neural plasticity; hippocampus; pyramidal neurons; adult mouse
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MDPI and ACS Style

Ambrogini, P.; Lattanzi, D.; Di Palma, M.; Ciacci, C.; Savelli, D.; Galati, C.; Gioacchini, A.M.; Pietrangelo, L.; Vallorani, L.; Protasi, F.; Cuppini, R. Calsequestrin Deletion Facilitates Hippocampal Synaptic Plasticity and Spatial Learning in Post-Natal Development. Int. J. Mol. Sci. 2020, 21, 5473. https://doi.org/10.3390/ijms21155473

AMA Style

Ambrogini P, Lattanzi D, Di Palma M, Ciacci C, Savelli D, Galati C, Gioacchini AM, Pietrangelo L, Vallorani L, Protasi F, Cuppini R. Calsequestrin Deletion Facilitates Hippocampal Synaptic Plasticity and Spatial Learning in Post-Natal Development. International Journal of Molecular Sciences. 2020; 21(15):5473. https://doi.org/10.3390/ijms21155473

Chicago/Turabian Style

Ambrogini, Patrizia, Davide Lattanzi, Michael Di Palma, Caterina Ciacci, David Savelli, Claudia Galati, Anna M. Gioacchini, Laura Pietrangelo, Luciana Vallorani, Feliciano Protasi, and Riccardo Cuppini. 2020. "Calsequestrin Deletion Facilitates Hippocampal Synaptic Plasticity and Spatial Learning in Post-Natal Development" International Journal of Molecular Sciences 21, no. 15: 5473. https://doi.org/10.3390/ijms21155473

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