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Lookup NU author(s): Professor Jenny ReadORCiD
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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.
Author(s): Hardingham NR, Bannister NJ, Read JCA, Fox KD, Hardingham GE, Jack JJB
Publication type: Article
Publication status: Published
Journal: Journal of Neuroscience
Year: 2006
Volume: 26
Issue: 23
Pages: 6337-6345
ISSN (print): 0270-6474
ISSN (electronic): 1529-2401
Publisher: Society for Neuroscience
URL: http://dx.doi.org/10.1523/JNEUROSCI.5128-05.2006
DOI: 10.1523/JNEUROSCI.5128-05.2006
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