Age-dependent requirement of AKAP150-anchored PKA and GluR2-lacking AMPA receptors in LTP

Yuan Lu, Margaret Allen, Amy R. Halt, Michael Weisenhaus, Robert F. Dallapiazza, Duane D. Hall, Yuriy M. Usachev, G. Stanley McKnight, Johannes W Hell

Research output: Contribution to journalArticlepeer-review

139 Scopus citations


Association of PKA with the AMPA receptor GluR1 subunit via the A kinase anchor protein AKAP150 is crucial for GluR1 phosphorylation. Mutating the AKAP150 gene to specifically prevent PKA binding reduced PKA within postsynaptic densities (>70%). It abolished hippocampal LTP in 7-12 but not 4-week-old mice. Inhibitors of PKA and of GluR2-lacking AMPA receptors blocked single tetanus LTP in hippocampal slices of 8 but not 4-week-old WT mice. Inhibitors of GluR2-lacking AMPA receptors also prevented LTP in 2 but not 3-week-old mice. Other studies demonstrate that GluR1 homomeric AMPA receptors are the main GluR2-lacking AMPA receptors in adult hippocampus and require PKA for their functional postsynaptic expression during potentiation. AKAP150-anchored PKA might thus critically contribute to LTP in adult hippocampus in part by phosphorylating GluR1 to foster postsynaptic accumulation of homomeric GluR1 AMPA receptors during initial LTP in 8-week-old mice.

Original languageEnglish (US)
Pages (from-to)4879-4890
Number of pages12
JournalEMBO Journal
Issue number23
StatePublished - Nov 28 2007
Externally publishedYes


  • AKAP
  • AMPA receptors
  • Calcium
  • PKA
  • Synapse

ASJC Scopus subject areas

  • Genetics
  • Cell Biology


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