Plasticity of calcium channels in dendritic spines
作者： Ryohei Yasuda , Bernardo L Sabatini , Karel Svoboda
DOI: 10.1038/NN1112
关键词:
摘要: Voltage-sensitive Ca2+ channels (VSCCs) constitute a major source of calcium ions in dendritic spines, but their function is unknown. Here we show that R-type VSCCs spines rat CA1 pyramidal neurons are depressed for at least 30 min after brief trains back-propagating action potentials. Populations single stochastically and synchronously, independent the parent dendrite other implying depression result signaling restricted to individual spines. Induction VSCC blocks theta-burst-induced long-term potentiation (LTP), indicating postsynaptic potentials can modulate synaptic plasticity by tuning VSCCs. requires [Ca2+] elevations activation L-type VSCCs, which activate Ca2+/calmodulin-dependent kinase II (CaMKII) cyclic adenosine monophosphate (cAMP)-dependent pathway. Given do not contribute measurably influx they must downstream effectors either directly through voltage-dependent conformational changes or via microdomains.
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