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

Abstract

Calcium (Ca 2+) is a major second messenger in the regulation of different forms of synaptic and intrinsic plasticity. Tightly organized in space and time, postsynaptic Ca 2+ transients trigger the activation of many distinct Ca 2+ signaling cascades, providing a means for a highly specific signal transduction and plasticity induction. High-resolution two-photon microscopy combined with highly sensitive synthetic Ca 2+ indicators in brain slices allowed for the quantification and analysis of postsynaptic Ca 2+ dynamics in great detail. Much of our current knowledge about postsynaptic Ca 2+ mechanisms is derived from studying Ca 2+ transients in the dendrites and spines of pyramidal neurons. However, postsynaptic Ca 2+ dynamics differ considerably among different cell types. In particular, distinct rules of postsynaptic Ca 2+ signaling and, accordingly, of Ca 2+-dependent plasticity operate in GABAergic interneurons. Here, I review recent progress in understanding the complex organization of postsynaptic Ca 2+ signaling and its relevance to several forms of long-term potentiation at excitatory synapses in cortical GABAergic interneurons. © 2012 The Author. European Journal of Neuroscience © 2012 Federation of European Neuroscience Societies and Blackwell Publishing Ltd.