Postsynaptic IP3 receptor-mediated Ca2+ release modulates synaptic transmission in hippocampal neurons

Paul T. Kelly, Roger L. MacKinnon, Roger V. Dietz, Brady J. Maher, J. Wang

Research output: Contribution to journalArticlepeer-review

10 Scopus citations


Ca2+-dependent mechanisms are important in regulating synaptic transmission. The results herein indicate that whole-cell perfusion of inositol 1,4,5-trisphosphate receptor (IP3R) agonists greatly enhanced excitatory postsynaptic current (EPSC) amplitudes in postsynaptic hippocampal CA1 neurons. IP3R agonist-mediated increases in synaptic transmission changed during development and paralleled age-dependent increases in hippocampal type-1 IP3Rs. IP3R agonist-mediated increases in EPSC amplitudes were inhibited by postsynaptic perfusion of inhibitors of Ca2+/calmodulin, PKC and Ca2+/calmodulin-dependent protein kinase II. Postsynaptic perfusion of inhibitors of smooth endoplasmic reticulum (SER) Ca2+-ATPases, which deplete intracellular Ca2+ stores, also enhanced EPSC amplitudes. Postsynaptic perfusion of the IP 3R agonist adenophostin (AdA) during subthreshold stimulation appeared to convert silent to active synapses; synaptic transmission at these active synapses was completely blocked by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). Postsynaptic IP3R-mediated Ca2+ release also produced a significant increase in spontaneous EPSC frequency. These results indicate that Ca2+ release from intracellular stores play a key role in regulating the function of postsynaptic AMPARs.

Original languageEnglish (US)
Pages (from-to)232-248
Number of pages17
JournalMolecular Brain Research
Issue number1-2
StatePublished - Apr 27 2005
Externally publishedYes


  • Ca/calmodulin-dependent protein kinase (CaM-KII)
  • Calcium (Ca)
  • Calmodulin (CaM)
  • Development
  • Hippocampus
  • Inositol 1,4,5-trisphosphate receptor (IPR)
  • Protein kinase c (PKC)
  • Synaptic plasticity
  • Synaptic transmission

ASJC Scopus subject areas

  • Molecular Biology
  • Cellular and Molecular Neuroscience


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