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Cited by 363Ion channel regulation and functionNeuroscience and Neuropharmacology ResearchCardiac electrophysiology and arrhythmias

Kv7/KCNQ/M and HCN/h, but not KCa2/SK channels, contribute to the somatic medium after‐hyperpolarization and excitability control in CA1 hippocampal pyramidal cells

Gu, Ning, Vervaeke, Koen, Hu, Hua, Storm, Johan F.·2005·The Journal of Physiology
DOI 10.1113/jphysiol.2005.086835
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Abstract

In hippocampal pyramidal cells, a single action potential (AP) or a burst of APs is followed by a medium afterhyperpolarization (mAHP, lasting ∼0.1 s). The currents underlying the mAHP are considered to regulate excitability and cause early spike frequency adaptation, thus dampening the response to sustained excitatory input relative to responses to abrupt excitation. The mAHP was originally suggested to be primarily caused by M‐channels (at depolarized potentials) and h‐channels (at more negative potentials), but not SK channels. In recent reports, however, the mAHP was suggested to be generated mainly by SK channels or only by h‐channels. We have now re‐examined the mechanisms underlying the mAHP and early spike frequency adaptation in CA1 pyramidal cells by using sharp electrode and whole‐cell recording in rat hippocampal slices. The specific M‐channel blocker XE991 (10 μ m) suppressed the mAHP following 1–5 APs evoked by current injection at −60 mV. XE991 also enhanced the excitability of the cell, i.e. increased the number of APs evoked by a constant depolarizing current pulse, reduced their rate of adaptation, enhanced the afterdepolarization and promoted bursting. Conversely, the M‐channel opener retigabine reduced excitability. The h‐channel blocker ZD7288 (4‐ethylphenylamino‐1,2‐dimethyl‐6‐methylaminopyrimidinium chloride; 10 μ m) fully suppressed the mAHP at −80 mV, but had little effect at −60 mV, whereas XE991 did not measurably affect the mAHP at −80 mV. Likewise, ZD7288 had little or no effect on excitability or adaptation during current pulses injected from −60 mV, but changed the initial discharge during depolarizing pulses injected from −80 mV. In contrast to previous reports, we found that blockade of Ca 2+‐activated K+ channels of the SK/K Ca type by apamin (100–400 n m) failed to affect the mAHP or adaptation. A computational model of a CA1 pyramidal cell predicted that M‐ and h‐channels will generate mAHPs in a voltage‐dependent manner, as indicated by the experiments. We conclude that M‐ and h‐channels generate the somatic mAHP in hippocampal pyramidal cells, with little or no net contribution from SK channels.

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Authors
Gu, N., Vervaeke, K., Hu, H., & Storm, J. F.
Affiliations
University of Oslo (NO)
ORCID
Venue
The Journal of Physiology
Publisher
Wiley
Published
2005-07-27
Volume
566
Issue
3
Pages
689-715
ISSN
  • 0022-3751 (ISSN-L)
  • 1469-7793
DOI
10.1113/jphysiol.2005.086835
OpenAlex
W2103156942
Cited by
363
References
92
Citations by year
2026: 11 · 2025: 12 · 2024: 13 · 2023: 14 · 2022: 16 · 2021: 14 · 2020: 19 · 2019: 24 · 2018: 22 · 2017: 11 · 2016: 13 · 2015: 22 · 2014: 17 · 2013: 12 · 2012: 24
FWCI
9.16
Type
journal article
Language
en
Open access
closed
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations
  • The Journal of Physiology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac electrophysiology and arrhythmias
Keywords
M-channels, H+ channel, small conductance calcium-activated potassium channels, CA1 pyramidal neurons, hippocampus, spike frequency adaptation, neuronal excitability, XE991, retigabine, ZD7288, apamin, computational model, burst firing, afterdepolarizations, voltage-gated potassium channels
MeSH terms
Action Potentials, Adaptation, Physiological, Animals, Biological Clocks, Feedback, Hippocampus, Ion Channels, Male, Potassium Channels, Ion Channel Gating, Rats, Wistar, Long-Term Potentiation, Pyramidal Cells, Potassium Channels, Voltage-Gated, Potassium Channels, Calcium-Activated, Rats, Small-Conductance Calcium-Activated Potassium Channels, KCNQ Potassium Channels, KCNQ1 Potassium Channel, Cyclic Nucleotide-Gated Cation Channels, Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels

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