| Literature DB >> 19357290 |
Lisa Topolnik1, Simon Chamberland, Joe-Guillaume Pelletier, Israeli Ran, Jean-Claude Lacaille.
Abstract
Activity-dependent regulation of synaptic inputs in neurons is controlled by highly compartmentalized and dynamic dendritic calcium signaling. Among multiple Ca(2+) mechanisms operating in neuronal dendrites, voltage-sensitive Ca(2+) channels (VSCCs) represent a major source of Ca(2+) influx; however, their use-dependent implication, regulation, and function in different types of central neurons remain widely unknown. Using two-photon microscopy to probe Ca(2+) 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 Ca(2+) transients. This potentiation of dendritic Ca(2+) signaling required mGluR5-induced intracellular Ca(2+) 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.Entities:
Mesh:
Year: 2009 PMID: 19357290 PMCID: PMC6665741 DOI: 10.1523/JNEUROSCI.0493-09.2009
Source DB: PubMed Journal: J Neurosci ISSN: 0270-6474 Impact factor: 6.167