Cited by 548Ion channel regulation and functionNeuroscience and Neuropharmacology ResearchCardiac electrophysiology and arrhythmias

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Calcium-dependent current generating the afterhyperpolarization of hippocampal neurons

Lancaster, B., Adams, P. R.·1986·Journal of Neurophysiology

DOI 10.1152/jn.1986.55.6.1268

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Abstract

A single-electrode voltage-clamp technique was employed on in vitro hippocampal slices to examine the membrane current responsible for the slow afterhyperpolarization (AHP) in CA1 pyramidal cells. This was achieved by using conventional procedures to evoke an AHP in current clamp, followed rapidly by a switch into voltage clamp (hybrid clamp). The AHP current showed a dependence on extracellular K+, which was close to that predicted for a K+ current by the Nernst equation. The AHP current could be blocked by Cd2+ or norepinephrine. Although the AHP current showed a requirement for voltage-dependent Ca2+ entry, the current did not show any clear intrinsic voltage dependence. Once activated, AHP current is not turned off by hyperpolarizing the membrane potential. The effects of norepinephrine, Cd2+, and tetraethylammonium (TEA) were used to identify an AHP current component to the outward current evoked by depolarizing voltage commands from holding potentials that approximate to the resting potential for these cells. The AHP current can contribute significantly to the outward current during the depolarizing command. Upon repolarization it is evident as a slow outward tail current. This slow tail current had the same time constant as AHP currents evoked by hybrid clamp. Fast components to the tail currents were also observed. These were sensitive to Cd2+ and TEA. They probably represent a voltage-sensitive gKCa, sometimes termed C-current. The strong sensitivity to voltage and TEA displayed by the conventionally described gKCa (IC) are properties inconsistent with the AHP. It seems likely that the AHP current (IAHP) represents a Ca2+-activated K+ current separate from IC and that these two currents coexist in the same cell.

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“…example, VGCC disruption affects calcium-activated potassium channels by reducing calcium influx, impairing their activation and leading to deficient potassium outflow during afterhyperpolarization, which results in increased neuronal excitability in CA1 pyramidal cells (Lancaster and Adams, 1986).”
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“However, such sAHP strongly contributes to the prolonged outward current component, reaching maximum amplitude over longer time courses of several hundred milliseconds (Lancaster and Adams, 1986).”
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Authors: Lancaster, B., & Adams, P. R.
ORCID: Adams, P. R.
Venue: Journal of Neurophysiology
Publisher: American Physiological Society
Published: 1986-06-01
Volume: 55
Issue: 6
Pages: 1268-1282
ISSN: 0022-3077 (ISSN-L)
1522-1598
DOI: 10.1152/jn.1986.55.6.1268
OpenAlex: W1876408798
Cited by: 547
References: 0
Citations by year: 2026: 1 · 2025: 1 · 2024: 4 · 2023: 4 · 2022: 2 · 2021: 5 · 2020: 4 · 2019: 8 · 2018: 6 · 2017: 5 · 2016: 4 · 2015: 3 · 2014: 1 · 2013: 7 · 2012: 11
FWCI: 9.16
Type: journal article
Language: en
Open access: closed
Locations: Journal of Neurophysiology (publishedVersion)
PubMed (publishedVersion)
Funders: National Institute of Neurological Disorders and Stroke (NS18579)
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: afterhyperpolarization, calcium-activated potassium current, CA1 pyramidal neurons, tetraethylammonium sensitivity, cadmium block, norepinephrine, voltage-gated potassium channels
MeSH terms: Action Potentials, Animals, Calcium, Hippocampus, Ion Channels, Kinetics, Neural Conduction, Synaptic Transmission, Potassium, Rats, In Vitro Techniques

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Calcium-dependent current generating the afterhyperpolarization of hippocampal neurons

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