Developmental switch in requirement for PKA RIIβ in NMDA-receptor-dependent synaptic plasticity at Schaffer collateral to CA1 pyramidal cell synapses

Yupeng Yang, Koichi Takeuchi, Alma Rodenas-Ruano, Yukihiro Takayasu, Michael V.L. Bennett, R. Suzanne Zukin

Research output: Contribution to journalArticle

19 Scopus citations


The cAMP/protein kinase A (PKA) signaling cascade is crucial for synaptic plasticity in a wide variety of species. PKA regulates Ca2+ permeation through NMDA receptors (NMDARs) and induction of NMDAR-dependent synaptic plasticity at the Schaffer collateral to CA1 pyramidal cell synapse. Whereas the role of PKA in induction of NMDAR-dependent LTP at CA1 synapses is established, the identity of PKA isoforms involved in this phenomenon is less clear. Here we report that protein synthesis-independent NMDAR-dependent LTP at the Schaffer collateral-CA1 synapse in the hippocampus is deficient, but NMDAR-dependent LTD is normal, in young (postnatal day 10 (P10)-P14) mice lacking PKA RIIβ, the PKA regulatory protein that links PKA to NMDARs at synaptic sites. In contrast, in young adult (P21-P28) mice lacking PKA RIIβ, LTP is normal and LTD is abolished. These findings indicate that distinct PKA isoforms may subserve distinct forms of synaptic plasticity and are consistent with a developmental switch in the signaling cascades required for LTP induction.

Original languageEnglish (US)
Pages (from-to)56-65
Number of pages10
Issue number1
StatePublished - Jan 1 2009



  • CA1 synapses
  • Hippocampus
  • Long-term depression
  • Long-term potentiation
  • NMDA receptors
  • PKA
  • PKA RIIβ knockout mice
  • PKA type II regulatory subunit
  • Synaptic plasticity

ASJC Scopus subject areas

  • Pharmacology
  • Cellular and Molecular Neuroscience

Cite this