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Calcium-dependent current generating the afterhyperpolarization of hippocampal neurons
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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“AHP currents are mainly mediated by calcium-dependent potassium channels [77, 78], but also partly by calcium-independent potassium channels [79].”
From Chronic unpredictable stress induces depression-related behaviors by suppressing AgRP neuron activity (2021) · cites this paper as [77]
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Metadata
- 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
- 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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