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.
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. lisa.topolnik@crulrg.ulaval.ca
Lisa
L
Topolnik
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D020013:Calcium Signaling / Q000502:physiology; D002540:Cerebral Cortex / Q000166:cytology*; D003712:Dendrites / Q000378:metabolism*; D059330:GABAergic Neurons / Q000166:cytology; D007395:Interneurons / Q000166:cytology*; D017774:Long-Term Potentiation / Q000502:physiology*; D009433:Neural Inhibition / Q000502:physiology*; D013569:Synapses / Q000502:physiology
D002118:Calcium