The Journal of Neuroscience, April 8, 2009, 29(14):4658-4663; doi:10.1523/JNEUROSCI.0493-09.2009
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Brief Communications
Activity-Dependent Compartmentalized Regulation of Dendritic Ca2+ Signaling in Hippocampal Interneurons
Lisa Topolnik,1,2,3
Simon Chamberland,1,3
Joe-Guillaume Pelletier,2
Israeli Ran,2 and
Jean-Claude Lacaille2
1Département de Biochimie et de Microbiologie, Faculté des Sciences et de Génie, Université Laval, Québec City, Québec, Canada G1V 0A6, 2Département de Physiologie, Groupe de Recherche sur le Système Nerveux Central, Université de Montréal, Montréal, Québec, Canada H3C 3J7, and 3Unite de Neurobiologie Cellulaire, Centre de Recherche Université Laval Robert-Giffard, Québec City, Québec, Canada G1J 2GS
Correspondence should be addressed to either of the following: Jean-Claude Lacaille, Département de Physiologie, Faculté de Médecine, Université de Montréal, Case Postale 6128, Succursale Centre-Ville, Montréal, Québec, Canada H3C 3J7, Email: jean-claude.lacaille{at}umontreal.ca; or Lisa Topolnik, Unite de Neurobiologie Cellulaire, CRULRG, 2601 Chemin de la Canardiere, Suite F-6530-2, Québec City, Québec, Canada G1J 2G3, Email: Lisa.Topolnik{at}crulrg.ulaval.ca
Activity-dependent regulation of synaptic inputs in neurons is controlled by highly compartmentalized and dynamic dendritic calcium signaling. Among multiple Ca2+ mechanisms operating in neuronal dendrites, voltage-sensitive Ca2+ channels (VSCCs) represent a major source of Ca2+ influx; however, their use-dependent implication, regulation, and function in different types of central neurons remain widely unknown. Using two-photon microscopy to probe Ca2+ signaling in dendrites of hippocampal oriens/alveus interneurons, we found that intense synaptic activity or local activation of mGluR5 induced long-lasting potentiation of action potential evoked Ca2+ transients. This potentiation of dendritic Ca2+ signaling required mGluR5-induced intracellular Ca2+ release and PKC activation and was expressed as a selective compartmentalized potentiation of L-type VSCCs. Thus, in addition to mGluR1a-dependent synaptic plasticity, hippocampal interneurons in the feedback inhibitory circuit demonstrate a novel form of mGluR5-induced dendritic plasticity. Given an implication of L-type VSCCs in the induction of Hebbian LTP at interneuron excitatory synapses, their activity-dependent regulation may represent a powerful mechanism for regulating synaptic plasticity.
Received Jan. 29, 2009;
accepted March 9, 2009.
Correspondence should be addressed to either of the following: Jean-Claude Lacaille, Département de Physiologie, Faculté de Médecine, Université de Montréal, Case Postale 6128, Succursale Centre-Ville, Montréal, Québec, Canada H3C 3J7, Email: jean-claude.lacaille{at}umontreal.ca; or Lisa Topolnik, Unite de Neurobiologie Cellulaire, CRULRG, 2601 Chemin de la Canardiere, Suite F-6530-2, Québec City, Québec, Canada G1J 2G3, Email: Lisa.Topolnik{at}crulrg.ulaval.ca