ArticleThe Journal of physiology1994
Photolytic manipulation of Ca2+ and the time course of slow, Ca(2+)-activated K+ current in rat hippocampal neurones.
Article in The Journal of physiology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 82 citations in OpenAlex.
- Photochemical Restoration of Light Sensitivity in the Degenerated Canine Retina.Pharmaceutics · 2022Article
- Deciphering Molecular Mechanisms and Intervening in Physiological and Pathophysiological Processes of CaCells · 2021Review
- The Molecular Basis for the Calcium-Dependent Slow Afterhyperpolarization in CA1 Hippocampal Pyramidal Neurons.Frontiers in physiology · 2021Review
- Similar nicotinic excitability responses across the developing hippocampal formation are regulated by small-conductance calcium-activated potassium channels.Journal of neurophysiology · 2018Article
- T-type channels buddy up.Pflugers Archiv : European journal of physiology · 2014Review
- A sodium-pump-mediated afterhyperpolarization in pyramidal neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- The calcium-activated slow AHP: cutting through the Gordian knot.Frontiers in cellular neuroscience · 2012Article
- Bidirectional pattern-specific plasticity of the slow afterhyperpolarization in rats: role for high-voltage activated Ca2+ channels and I h.The European journal of 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
- 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
- Alterations in Ca2+-buffering in prion-null mice: association with reduced afterhyperpolarizations in CA1 hippocampal neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
- A model for synaptic development regulated by NMDA receptor subunit expression.Journal of computational neuroscience · 2008Article
- 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
- Hippocalcin: a new solution to an old puzzle.Neuron · 2007Article
- Activation kinetics of the slow afterhyperpolarization in hippocampal CA1 neurons.Pflugers Archiv : European journal of physiology · 2004Article
- Novel action of BAPTA series chelators on intrinsic K+ currents in rat hippocampal neurones.The Journal of physiology · 2000Article
- Gating properties of single SK channels in hippocampal CA1 pyramidal neurons.Biophysical journal · 1999Article
- Calcium regulation of a slow post-spike hyperpolarization in vagal afferent neurons.Proceedings of the National Academy of Sciences of the United States of America · 1999Article
- Calcium-activated potassium conductances contribute to action potential repolarization at the soma but not the dendrites of hippocampal CA1 pyramidal neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1999Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
1. Experiments were performed on hippocampal CA1 pyramidal cells to investigate the time course of a slow, Ca(2+)-activated K+ current that follows a burst of action potentials. At a temperature of 27-30 degrees C, this current rises to a peak 200-400 ms following the cessation of Ca2+ entry before decaying to baseline in 4-8s. 2. Intracellular recordings were made using electrodes containing the photolabile calcium buffers nitr-5 or DM-nitrophen loaded appropriately with Ca2+. Under these conditions, photolysis of the compound using an ultraviolet flashlamp caused an instantanous increase in cytoplasmic Ca2+ throughout the cell. The response to flash photolysis was a membrane hyperpolarization with an onset limited by the membrane time constant. Multiple (up to twenty) flash responses could be generated. 3. The postspike slow after-hyperpolarization (AHP) and flash-induced hyperpolarizations showed a common sensitivity to the beta-adrenergic receptor agonist isoprenaline. 4. Following a burst of spikes, the current underlying an AHP in progress could be terminated or reduced by photolysis-induced production of calcium buffer from diazo-4 within the cell. This action was rapid (within the setting time of the flash artifact, i.e. < 10 ms) despite the fact that the manipulation occurred 400-500 ms following the end of Ca2+ entry. 5. Partial block of the slow AHP by buffer production was accompanied by an increase in the time to peak of the event. 6. The time to peak of the slow AHP could also be manipulated by experiments which altered the spatial distribution of Ca2+ entry, such as production of calcium spikes or dendritic depolarization by glutamate in the presence of tetrodotoxin. 7. The Ca(2+)-dependent K+ current responsible for the slow AHP responds immediately to increase or decreases in cytoplasmic Ca2+. It seems likely, therefore, that the slow AHP is controlled solely by changes in free Ca2+ and that the time course is governed by the redistribution of cytoplasmic Ca2+ following activity-induced entry through voltage- or receptor-operated channels.
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