Article abstract
Nature Neuroscience 12, 577 - 584 (2009)
Published online: 12 April 2009 | doi:10.1038/nn.2307
HCN hyperpolarization-activated cation channels inhibit EPSPs by interactions with M-type K+ channels
Meena S George1, L F Abbott1,2 & Steven A Siegelbaum1,3,4
Abstract
The processing of synaptic potentials by neuronal dendrites depends on both their passive cable properties and active voltage-gated channels, which can generate complex effects as a result of their nonlinear properties. We characterized the actions of HCN (hyperpolarization-activated cyclic nucleotide-gated cation) channels on dendritic processing of subthreshold excitatory postsynaptic potentials (EPSPs) in mouse CA1 hippocampal neurons. The HCN channels generated an excitatory inward current (Ih) that exerted a direct depolarizing effect on the peak voltage of weak EPSPs, but produced a paradoxical hyperpolarizing effect on the peak voltage of stronger, but still subthreshold, EPSPs. Using a combined modeling and experimental approach, we found that the inhibitory action of Ih was caused by its interaction with the delayed-rectifier M-type K+ current. In this manner, Ih can enhance spike firing in response to an EPSP when spike threshold is low and can inhibit firing when spike threshold is high.
- Department of Neuroscience, Columbia University, New York, New York, USA.
- Departments of Physiology and Cellular Biophysics, Columbia University, New York, New York, USA.
- Department of Pharmacology, Columbia University, New York, New York, USA.
- Howard Hughes Medical Institute, Columbia University, New York, New York, USA.
Correspondence to: Steven A Siegelbaum1,3,4 e-mail: sas8@columbia.edu
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