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Long-Term Memory Deficits in Pavlovian Fear Conditioning in Ca2+/Calmodulin Kinase Kinase α-Deficient Mice

Mol. Cell. Biol., 1 December 2006
Vol. 26, Issue 23, p. 9105-9115
DOI: 10.1128/MCB.01452-06

Long-Term Memory Deficits in Pavlovian Fear Conditioning in Ca2+/Calmodulin Kinase Kinase α-Deficient Mice

  1. Frank Blaeser1,
  2. Matthew J. Sanders2,
  3. Nga Truong3,
  4. Shanelle Ko4,
  5. Long Jun Wu4,
  6. David F. Wozniak5,
  7. Michael S. Fanselow2,
  8. Min Zhuo4 and
  9. Talal A. Chatila3,*
  1. 1Institute of Transfusion Medicine, University of Leipzig, Leipzig, Germany
  2. 2Department of Psychology, University of California at Los Angeles, Los Angeles, California 90095
  3. 3Department of Pediatrics, The David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California 90095
  4. 4Department of Physiology, University of Toronto, Toronto, Ontario, Canada M5S 1A8
  5. 5Department of Psychiatry, Washington University School of Medicine, St. Louis, Missouri 63110

ABSTRACT

Signaling by the Ca2+/calmodulin kinase (CaMK) cascade has been implicated in neuronal gene transcription, synaptic plasticity, and long-term memory consolidation. The CaM kinase kinase α (CaMKKα) isoform is an upstream component of the CaMK cascade whose function in different behavioral and learning and memory paradigms was analyzed by targeted gene disruption in mice. CaMKKα mutants exhibited normal long-term spatial memory formation and cued fear conditioning but showed deficits in context fear during both conditioning and long-term follow-up testing. They also exhibited impaired activation of the downstream kinase CaMKIV/Gr and its substrate, the transcription factor cyclic AMP-responsive element binding protein (CREB) upon fear conditioning. Unlike CaMKIV/Gr-deficient mice, the CaMKKα mutants exhibited normal long-term potentiation and normal levels of anxiety-like behavior. These results demonstrate a selective role for CaMKKα in contextual fear memory and suggest that different combinations of upstream and downstream components of the CaMK cascade may serve distinct physiological functions.

FOOTNOTES

    • Received 6 August 2006.
    • Returned for modification 29 August 2006.
    • Accepted 18 September 2006.
  • *Corresponding author. Mailing address: Department of Pediatrics, The David Geffen School of Medicine, University of California at Los Angeles, 10833 Le Conte Avenue, Los Angeles, CA 90095-1752. Phone: (310) 825-4125. Fax: (310) 206-4584. E-mail: Tchatila{at}mednet.ucla.edu.
  • Published ahead of print on 2 October 2006.

Citation:

F. Blaeser, M. J. Sanders, N. Truong, S. Ko, L. J. Wu, D. F. Wozniak, M. S. Fanselow, M. Zhuo, and T. A. Chatila, Long-Term Memory Deficits in Pavlovian Fear Conditioning in Ca2+/Calmodulin Kinase Kinase α-Deficient Mice. Mol. Cell. Biol. 26, 9105-9115 (2006).

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