Trace eyeblink conditioning requires the hippocampus but not autophosphorylation of αCaMKII in mice

Masuo Ohno*, Wilbur Tseng, Alcino J. Silva, John F. Disterhoft

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

21 Scopus citations

Abstract

Little is known about signaling mechanisms underlying temporal associative learning. Here, we show that mice with a targeted point mutation that prevents autophosphorylation of αCaMKII (αCaMKIIT286A) learn trace eyeblink conditioning normally. This forms a sharp contrast to the severely impaired spatial learning in the water maze and contextual fear conditioning observed in αCaMKIIT286A mutants. Importantly, hippocampal lesions impaired trace eyeblink conditioning in αCaMKIIT286A mice, suggesting a potential role of hippocampal αCaMKII-independent mechanisms. These results indicate that hippocampal signaling mechanisms that underlie temporal associative learning as assessed by trace eyeblink conditioning may differ from those of spatial and contextual learning.

Original languageEnglish (US)
Pages (from-to)211-215
Number of pages5
JournalLearning and Memory
Volume12
Issue number3
DOIs
StatePublished - May 2005

ASJC Scopus subject areas

  • Neuropsychology and Physiological Psychology
  • Cognitive Neuroscience
  • Cellular and Molecular Neuroscience

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