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Calcium Release Mediated by Redox-Sensitive RyR2 Channels Has a Central Role in Hippocampal Structural Plasticity and Spatial Memory
Author(s) -
Jamileth More,
Bárbara Bruna,
Pedro Lobos,
José Luis Galaz,
Paula Figueroa,
Silvia Namias,
Gina Sánchez,
Genaro Barrientos,
José L. Valdés,
Andrea Paula-Lima,
Cecilia Hidalgo,
Tatiana Adasme
Publication year - 2018
Publication title -
antioxidants and redox signaling
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.277
H-Index - 190
eISSN - 1557-7716
pISSN - 1523-0864
DOI - 10.1089/ars.2017.7277
Subject(s) - ryanodine receptor , downregulation and upregulation , ryanodine receptor 2 , chemistry , microbiology and biotechnology , hippocampal formation , biology , neuroscience , receptor , biochemistry , gene
Previous studies indicate that hippocampal synaptic plasticity and spatial memory processes entail calcium release from intracellular stores mediated by ryanodine receptor (RyR) channels. In particular, RyR-mediated Ca 2+ release is central for the dendritic spine remodeling induced by brain-derived neurotrophic factor (BDNF), a neurotrophin that stimulates complex signaling pathways leading to memory-associated protein synthesis and structural plasticity. To examine if upregulation of ryanodine receptor type-2 (RyR2) channels and the spine remodeling induced by BDNF entail reactive oxygen species (ROS) generation, and to test if RyR2 downregulation affects BDNF-induced spine remodeling and spatial memory.

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