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HCN hyperpolarization-activated cation channels inhibit EPSPs by interactions with M-type K+ channels

Summary: 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
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 K1 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.
Neurons actively process and integrate synaptic potentials through the
actions of a wide array of voltage-gated ion channels that are often
differentially expressed throughout a neuron's dendritic tree1. In some
instances, the effects of voltage-gated channels on dendritic processing
are relatively straightforward and well understood. For example,
dendritic voltage-gated sodium and calcium channels can amplify
synaptic potentials2 through the generation of local or propagated
dendritic action potentials3,4. In contrast, dendritic voltage-gated or
calcium-activated K+ channels can reduce EPSP amplitude and dam-


Source: Abbott, Laurence - Center for Neurobiology and Behavior & Department of Physiology and Cellular Biophysics, Columbia University
Lazar, Aurel A. - Department of Electrical Engineering, Columbia University


Collections: Biology and Medicine; Computer Technologies and Information Sciences