Abstract
To evaluate the role in synaptic plasticity of ryanodine receptor type 3 ( RyR3), which is normally enriched in hippocampal area CA1, we generated RyR3-deficient mice. Mutant mice exhibited facilitated CA1 long-term potentiation (LTP) induced by short tetanus (100 Hz, 100 ms) stimulation. Unlike LTP in wild-type mice, this LTP was not blocked by the NMDA receptor antagonist D-AP5 but was partially dependent on L-type voltage-dependent Ca 2+ channels (VDCCs) and metabotropic glutamate receptors (mGluRs). Long-term depression (LTD) was not induced in RyR3-deficient mice. RyR3-deficient mice also exhibited improved spatial learning on a Morris water maze task. These results suggest that in wild-type mice, in contrast to the excitatory role of Ca 2+ influx, RyR3-mediated intracellular Ca 2+ ([Ca 2+] i) release from endoplasmic reticulum (ER) may inhibit hippocampal LTP and spatial learning.
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