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The Journal of Neuroscience, June 15, 2005, 25(24):5763-5773; doi:10.1523/JNEUROSCI.0624-05.2005
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Cellular/Molecular
R-Type Calcium Channels Contribute to Afterdepolarization and Bursting in Hippocampal CA1 Pyramidal Neurons
Alexia E. Metz,1 * Tim Jarsky,1 * Marco Martina,1,3 andNelson Spruston1,2 1Northwestern University Institute for Neuroscience and 2Department of Neurobiology and Physiology, Northwestern University, Evanston, Illinois 60208, and 3Department of Physiology, Feinberg School of Medicine, Chicago, Illinois 60611
Action potentials in pyramidal neurons are typically followed by an afterdepolarization (ADP), which in many cells contributes to intrinsic burst firing. Despite the ubiquity of this common excitable property, the responsible ion channels have not been identified. Using current-clamp recordings in hippocampal slices, we find that the ADP in CA1 pyramidal neurons is mediated by an Ni2+-sensitive calcium tail current. Voltage-clamp experiments indicate that the Ni2+-sensitive current has a pharmacological and biophysical profile consistent with R-type calcium channels. These channels are available at the resting potential, are activated by the action potential, and remain open long enough to drive the ADP. Because the ADP correlates directly with burst firing in CA1 neurons, R-type calcium channels are crucial to this important cellular behavior, which is known to encode hippocampal place fields and enhance synaptic plasticity.
Key words: ADP; intrinsic excitability; nickel; patch clamp; afterhyperpolarization; persistent sodium current
Received Oct 1, 2004; revised May 6, 2005; accepted May 8, 2005.
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