Dendritic calcium mechanisms and long-term potentiation in cortical inhibitory interneurons


  • Lisa Topolnik

    1. Department of Biochemistry, Microbiology and Bio-informatics, Université Laval, Axis of Cellular and Molecular Neurosciences, 2601 Ch. De La Canardière, CRIUSMQ, Québec city, QC, PQ, G1J 2G3, Canada
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Lisa Topolnik, as above.


Calcium (Ca2+) is a major second messenger in the regulation of different forms of synaptic and intrinsic plasticity. Tightly organized in space and time, postsynaptic Ca2+ transients trigger the activation of many distinct Ca2+ signaling cascades, providing a means for a highly specific signal transduction and plasticity induction. High-resolution two-photon microscopy combined with highly sensitive synthetic Ca2+ indicators in brain slices allowed for the quantification and analysis of postsynaptic Ca2+ dynamics in great detail. Much of our current knowledge about postsynaptic Ca2+ mechanisms is derived from studying Ca2+ transients in the dendrites and spines of pyramidal neurons. However, postsynaptic Ca2+ dynamics differ considerably among different cell types. In particular, distinct rules of postsynaptic Ca2+ signaling and, accordingly, of Ca2+-dependent plasticity operate in GABAergic interneurons. Here, I review recent progress in understanding the complex organization of postsynaptic Ca2+ signaling and its relevance to several forms of long-term potentiation at excitatory synapses in cortical GABAergic interneurons.