Nature Neuroscience6, 948 - 955 (2003)
Published online: 24 August 2003; | doi:10.1038/nn1112
Plasticity of calcium channels in dendritic spines
Ryohei Yasuda1, Bernardo L Sabatini1, 2
& Karel Svoboda1
1
Howard Hughes Medical Institute, Cold Spring Harbor Laboratory, 1 Bungtown Road Cold Spring Harbor, New York 11724, USA.
2
Present address: Department of Neurobiology, Harvard Medical School, 220 Longwood Avenue, Boston, Massachusetts 02115, USA.
Correspondence should be addressed to Karel Svoboda svoboda@cshl.org
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 in spines of rat CA1 pyramidal neurons are depressed for at least 30 min after brief trains of back-propagating action potentials. Populations of channels in single spines are depressed stochastically and synchronously, independent of channels in the parent dendrite and other spines, implying that depression is the result of signaling restricted to individual spines. Induction of VSCC depression blocks theta-burst-induced long-term potentiation (LTP), indicating that postsynaptic action potentials can modulate synaptic plasticity by tuning VSCCs. Induction of depression requires [Ca2+] elevations and activation of L-type VSCCs, which activate Ca2+/calmodulin-dependent kinase II (CaMKII) and a cyclic adenosine monophosphate (cAMP)-dependent pathway. Given that L-type VSCCs do not contribute measurably to Ca2+ influx in spines, they must activate downstream effectors either directly through voltage-dependent conformational changes or via [Ca2+] microdomains.
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