Incremental generation of an EST set for the analysis of scrapie pathogenesis.

Anton Gossner, John Hopkins

Research output: Contribution to journalArticlepeer-review

Abstract / Description of output

Bursts of synaptic transmission are known to induce transient depletion of Ca2+ within the synaptic cleft. Although Ca2+ depletion has been shown to lower presynaptic release probability, effects on the postsynaptic cell have not been reported. In this study, we show that physiologically relevant reductions in extracellular Ca2+ lead to a decrease in synaptic strength between synaptically coupled layer 2/3 cortical pyramidal neurons. Using quantal analysis and mEPSP analysis, we demonstrate that a lowered extracellular Ca2+ produces a reduction in the postsynaptic quantal size in addition to its known effect on release probability. An elevated Mg2+ level can prevent this reduction in postsynaptic efficacy at subphysiological Ca2+ levels. We show that the calcium-dependent effect on postsynaptic quantal size is mediated by group 1 metabotropic glutamate receptors, acting via CaMKII (Ca2+/calmodulin-dependent protein kinase II) and PKC. Therefore, physiologically relevant changes in extracellular Ca2+ can regulate information transfer at cortical synapses via both presynaptic and postsynaptic mechanisms.
Original languageEnglish
Pages (from-to)75-78
Number of pages4
JournalSmall Ruminant Research
Issue number1
Publication statusPublished - 2008

Keywords / Materials (for Non-textual outputs)

  • Animals
  • Calcium/metabolism/ physiology
  • Excitatory Postsynaptic Potentials
  • Extracellular Space/ metabolism
  • Magnesium/metabolism
  • Osmolar Concentration
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, Metabotropic Glutamate/ physiology
  • Synapses/ physiology


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