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 journalArticlepeer-review


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
Issue number17
StatePublished - Sep 1 2000


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

ASJC Scopus subject areas

  • Neuroscience(all)

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