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

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.