학술논문

HCN hyperpolarization-activated cation channels inhibit EPSPs by interactions with M-type [K.sup.+] channels
Document Type
Report
Source
Nature Neuroscience. May, 2009, Vol. 12 Issue 5, p577, 8 p.
Subject
United States
Language
English
ISSN
1097-6256
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 ([I.sub.h]) 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 [I.sub.h] was caused by its interaction with the delayed-rectifier M-type [K.sup.+] current. In this manner, [I.sub.h] 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 tree (1). In [...]