Deletion of the ryanodine receptor type 3 (RyR3) impairs forms of synaptic plasticity and spatial learning

Detlef Balschun, David P. Wolfer, Federica Bertocchini, Virginia Barone, Antonio Conti, Werner Zuschratter, Ludwig Missiaen, Hans Peter Lipp, J. Uwe Frey, Vincenzo Sorrentino

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147 Scopus citations


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 relearning 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 Ca2+ release in the intracellular processes underlying spatial learning and hippocampal synaptic plasticity.

Original languageEnglish (US)
Pages (from-to)5264-5273
Number of pages10
JournalEMBO Journal
Issue number19
StatePublished - Oct 1 1999
Externally publishedYes


  • Behavior
  • Calcium release channe]s
  • Ryanodine receptor type 3
  • Spatial learning
  • Synaptic plasticity

ASJC Scopus subject areas

  • Neuroscience(all)
  • Molecular Biology
  • Biochemistry, Genetics and Molecular Biology(all)
  • Immunology and Microbiology(all)


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