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Deletion of the ryanodine receptor type 3 (RyR3) impairs forms of synaptic plasticity and spatial learning
Author(s) -
Balschun Detlef,
Wolfer David P.,
Bertocchini Federica,
Barone Virginia,
Conti Antonio,
Zuschratter Werner,
Missiaen Ludwig,
Lipp HansPeter,
Frey J. Uwe,
Sorrentino Vincenzo
Publication year - 1999
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1093/emboj/18.19.5264
Subject(s) - biology , ryanodine receptor , synaptic plasticity , plasticity , receptor , microbiology and biotechnology , neuroscience , biochemistry , physics , thermodynamics
Deletion of the ryanodine receptor type 3 (RyR3) results in specific changes in hippocampal synaptic plasticity, without affecting hippocampal morphology, basal synaptic transmission or presynaptic function. Robust long‐term potentiation (LTP) induced by repeated, strong tetanization in the CA1 region and in the dentate gyrus was unaltered in hippocampal slices in vitro , whereas weak forms of plasticity generated by either a single weak tetanization or depotentiation of a robust LTP were impaired. These distinct physiological deficits were paralleled by a reduced flexibility in re‐learning a new target in the water‐maze. In contrast, learning performance in the acquisition phase and during probe trial did not differ between the mutants and their wild‐type littermates. In the open‐field, RyR3 −/− mice displayed a normal exploration and habituation, but had an increased speed of locomotion and a mild tendency to circular running. The observed physiological and behavioral effects implicate RyR3‐mediated Ca 2+ release in the intracellular processes underlying spatial learning and hippocampal synaptic plasticity.