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CAKß/Pyk2 kinase is a signaling link for induction of long-term potentiation in CA1 hippocampus
Neuron
  • Yueqiao Huang, Philadelphia College of Osteopathic Medicine
  • Wei-Yang Lu
  • Declan W. Ali
  • Kenneth A. Pelkey
  • Graham M. Pitcher
  • You Ming Lu
  • Hiroshi Aoto
  • John C. Roder
  • Terukatsu Sasaki
  • Michael W. Salter
Document Type
Article
Publication Date
1-1-2001
Abstract
Long-term potentiation (LTP) is an activity-dependent enhancement of synaptic efficacy, considered a model of learning and memory. The biochemical cascade producing LTP requires activation of Src, which upregulates the function of NMDA receptors (NMDARs), but how Src becomes activated is unknown. Here, we show that the focal adhesion kinase CAKß/Pyk2 upregulated NMDAR function by activating Src in CA1 hippocampal neurons. Induction of LTP was prevented by blocking CAKß/Pyk2, and administering CAKß/Pyk2 intracellularly mimicked and occluded LTP. Tyrosine phosphorylation of CAKß/Pyk2 and its association with Src was increased by stimulation that produced LTP. Finally, CAKß/Pyk2-stimulated enhancement of synaptic AMPA responses was prevented by blocking NMDARS, chelating intracellular Ca2+, or blocking Src. Thus, activating CAKß/Pyk2 is required for inducing LTP and may depend upon downstream activation of Src to upregulate NMDA receptors.
Comments

This article was published in Neuron, Volume 29, Issue 2, Pages 485-496.

The published version is available at http://dx.doi.org/10.1016/S0896-6273(01)00220-3.

Copyright © 2001 Elsevier and distributed under user license.

Citation Information
Yueqiao Huang, Wei-Yang Lu, Declan W. Ali, Kenneth A. Pelkey, et al.. "CAKß/Pyk2 kinase is a signaling link for induction of long-term potentiation in CA1 hippocampus" Neuron Vol. 29 Iss. 2 (2001) p. 485 - 496
Available at: http://works.bepress.com/yue-qiaogeorge_huang/11/