ArticlePflugers Archiv : European journal of physiology2004
Activation kinetics of the slow afterhyperpolarization in hippocampal CA1 neurons.
Article in Pflugers Archiv : European journal of physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- Modeling Time Cell Neuron-Level Dynamics.Computational brain & behavior · 2024Article
- An in silico and in vitro human neuronal network model reveals cellular mechanisms beyond NaStem cell reports · 2023Article
- The Molecular Basis for the Calcium-Dependent Slow Afterhyperpolarization in CA1 Hippocampal Pyramidal Neurons.Frontiers in physiology · 2021Review
- Transient Hypoxemia Disrupts Anatomical and Functional Maturation of Preterm Fetal Ovine CA1 Pyramidal Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- βJournal of neurophysiology · 2019Article
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- High-fat diet impairs spatial memory and hippocampal intrinsic excitability and sex-dependently alters circulating insulin and hippocampal insulin sensitivity.Biology of sex differences · 2016Article
- Distinct Ca2+ sources in dendritic spines of hippocampal CA1 neurons couple to SK and Kv4 channels.Neuron · 2014Article
- Article
- A sodium-pump-mediated afterhyperpolarization in pyramidal neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- A small conductance calcium-activated K+ channel in C. elegans, KCNL-2, plays a role in the regulation of the rate of egg-laying.PloS one · 2013Article
- The calcium-activated slow AHP: cutting through the Gordian knot.Frontiers in cellular neuroscience · 2012Article
- Visinin-like neuronal calcium sensor proteins regulate the slow calcium-activated afterhyperpolarizing current in the rat cerebral cortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- The KCNQ5 potassium channel mediates a component of the afterhyperpolarization current in mouse hippocampus.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Nonequilibrium calcium dynamics regulate the autonomous firing pattern of rat striatal cholinergic interneurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- Control of IsAHP in mouse hippocampus CA1 pyramidal neurons by RyR3-mediated calcium-induced calcium release.Pflugers Archiv : European journal of physiology · 2007Article
- Hippocalcin gates the calcium activation of the slow afterhyperpolarization in hippocampal pyramidal cells.Neuron · 2007Article
- Ca2+ -activated K+ channels of the BK-type in the mouse brain.Histochemistry and cell biology · 2006Article
- Small conductance Ca2+-activated K+ channel knock-out mice reveal the identity of calcium-dependent afterhyperpolarization currents.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004Article
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3 authors.
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Abstract
The activation of the slow afterhyperpolarization (sAHP) in CA1 neurons was studied using whole-cell recordings in the presence of inhibitors of the fast and medium-duration AHPs. The amplitude of the slow afterhyperpolarization current (IsAHP) increased as a function of duration and magnitude of the depolarizing voltage pulse reflecting graded increases in Ca(2+) influx through voltage-dependent Ca(2+) channels. Therefore, the time constant for activation, tau(max), determined from a family of IsAHPs as a function of pulse duration, was voltage dependent decreasing several-fold within the range of -20 to 20 mV and was dependent on extracellular [Ca(2+)]. The IsAHP displayed a pronounced rising phase that was well fit by a single exponential with a time constant, tau(rise), that was invariant of pulse duration, voltage, IsAHP amplitude, or external [Ca(2+)] and was significantly slower than the tau(max). In current clamp, the magnitude of the sAHP increased with the number of evoked action potentials, yet tau(rise) of the sAHP was invariant of action potential number and was similar to the tau(rise) of the IsAHP recorded in voltage-clamp. The results suggest that there are two components to the development of the IsAHP, a rapid, voltage- and Ca(2+)-dependent step, the magnitude and rate of which reflects the voltage dependence of the Ca(2+) channels, that triggers a second rate-limiting, voltage-independent process that dictates the slow IsAHP rise kinetics.
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