Impaired synaptic plasticity and cAMP response element-binding protein activation in Ca2+/calmodulin-dependent protein kinase type IV/Gr-Deficient mice

Nga Ho, Jason A. Liauw, Frank Blaeser, Feng Wei, Silva Hanissian, Lisa M. Muglia, David F. Wozniak, Anthony Nardi, Kara L. Arvin, David M. Holtzman, David J Linden, Min Zhuo, Louis J. Muglia, Talal A. Chatila

Research output: Contribution to journalArticle

Abstract

The Ca2+/calmodulin-dependent protein kinase type IV/Gr (CaMKIV/Gr) is a key effector of neuronal Ca2+ signaling; its function was analyzed by targeted gene disruption in mice. CaMKIV/Gr-deficient mice exhibited impaired neuronal cAMP-responsive element binding protein (CREB) phosphorylation and Ca2+/CREB-dependent gene expression. They were also deficient in two forms of synaptic plasticity: Long-term potentiation (LTP) in hippocampal CA1 neurons and a late phase of long-term depression in cerebellar Purkinje neurons. However, despite impaired LTP and CREB activation, CaMKIV/Gr-deficient mice exhibited no obvious deficits in spatial learning and memory. These results support an important role for CaMKIV/Gr in Ca2+-regulated neuronal gene transcription and synaptic plasticity and suggest that the contribution of other signaling pathways may spare spatial memory of CaMKIV/Gr-deficient mice.

Original languageEnglish (US)
Pages (from-to)6459-6472
Number of pages14
JournalJournal of Neuroscience
Volume20
Issue number17
Publication statusPublished - Sep 1 2000

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Keywords

  • Calcium/calmodulin-dependent kinase
  • CREB
  • LTD
  • LTP
  • Memory
  • Synaptic plasticity

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Ho, N., Liauw, J. A., Blaeser, F., Wei, F., Hanissian, S., Muglia, L. M., ... Chatila, T. A. (2000). Impaired synaptic plasticity and cAMP response element-binding protein activation in Ca2+/calmodulin-dependent protein kinase type IV/Gr-Deficient mice. Journal of Neuroscience, 20(17), 6459-6472.