ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1999
Photolytic manipulation of [Ca2+]i reveals slow kinetics of potassium channels underlying the afterhyperpolarization in hippocampal pyramidal neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed.
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- Deciphering Molecular Mechanisms and Intervening in Physiological and Pathophysiological Processes of CaCells · 2021Review
- Spatial information transfer in hippocampal place cells depends on trial-to-trial variability, symmetry of place-field firing, and biophysical heterogeneities.Neural networks : the official journal of the International Neural Network Society · 2021Article
- The Molecular Basis for the Calcium-Dependent Slow Afterhyperpolarization in CA1 Hippocampal Pyramidal Neurons.Frontiers in physiology · 2021Review
- Article
- Degeneracy in the robust expression of spectral selectivity, subthreshold oscillations, and intrinsic excitability of entorhinal stellate cells.Journal of neurophysiology · 2018Article
- Phosphatidylinositol 4,5-bisphosphate (PIPThe Journal of physiology · 2017Article
- Analogous synaptic plasticity profiles emerge from disparate channel combinations.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Incorporation of inwardly rectifying AMPA receptors at silent synapses during hippocampal long-term potentiation.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2014Article
- A sodium-pump-mediated afterhyperpolarization in pyramidal neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Hippocalcin and KCNQ channels contribute to the kinetics of the slow afterhyperpolarization.Biophysical journal · 2012Article
- The calcium-activated slow AHP: cutting through the Gordian knot.Frontiers in cellular neuroscience · 2012Article
- Stochastic amplification of calcium-activated potassium currents in Ca2+ microdomains.Journal of computational neuroscience · 2011Article
- Location and function of the slow afterhyperpolarization channels in the basolateral amygdala.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Dendritic spikes amplify the synaptic signal to enhance detection of motion in a simulation of the direction-selective ganglion cell.PLoS computational biology · 2010Article
- Two slow calcium-activated afterhyperpolarization currents control burst firing dynamics in gonadotropin-releasing hormone neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Locally balanced dendritic integration by short-term synaptic plasticity and active dendritic conductances.Journal of neurophysiology · 2009Article
- 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
- The BK-mediated fAHP is modulated by learning a hippocampus-dependent task.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
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2 authors.
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Abstract
The identity of the potassium channel underlying the slow, apamin-insensitive component of the afterhyperpolarization current (sIAHP) remains unknown. We studied sIAHP in CA1 pyramidal neurons using simultaneous whole-cell recording, calcium fluorescence imaging, and flash photolysis of caged compounds. Intracellular calcium concentration ([Ca2+]i) peaked earlier and decayed more rapidly than sIAHP. Loading cells with low concentrations of the calcium chelator EGTA slowed the activation and decay of sIAHP. In the presence of EGTA, intracellular calcium decayed with two time constants. When [Ca2+]i was increased rapidly after photolysis of DM-Nitrophen, both apamin-sensitive and apamin-insensitive outward currents were activated. The apamin-sensitive current activated rapidly (<20 msec), whereas the apamin-insensitive current activated more slowly (180 msec). The apamin-insensitive current was reduced by application of serotonin and carbachol, confirming that it was caused by sIAHP channels. When [Ca2+]i was decreased rapidly via photolysis of diazo-2, the decay of sIAHP was similar to control (1. 7 sec). All results could be reproduced by a model potassium channel gated by calcium, suggesting that the channels underlying sIAHP have intrinsically slow kinetics because of their high affinity for calcium.
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