Hyperpolarization-activated cation channels inhibit EPSPs by interactions with M-type K+ channels
| Autor: | Meena S. George, Steven A. Siegelbaum, L. F. Abbott |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2009 |
| Předmět: |
0303 health sciences
Chemistry Subthreshold conduction General Neuroscience musculoskeletal neural and ocular physiology Depolarization Neurotransmission Hyperpolarization (biology) Inhibitory postsynaptic potential Potassium channel Article 03 medical and health sciences 0302 clinical medicine medicine.anatomical_structure nervous system Excitatory postsynaptic potential medicine Neuron Neuroscience 030217 neurology & neurosurgery 030304 developmental biology |
| Zdroj: | Nature neuroscience |
| ISSN: | 1546-1726 1097-6256 |
| Popis: | 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(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(h) was caused by its interaction with the delayed-rectifier M-type K(+) current. In this manner, I(h) can enhance spike firing in response to an EPSP when spike threshold is low and can inhibit firing when spike threshold is high. |
| Databáze: | OpenAIRE |
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