You are not currently logged in.
Access JSTOR through your library or other institution:
If You Use a Screen ReaderThis content is available through Read Online (Free) program, which relies on page scans. Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
An Apamin-Sensitive Ca2+-activated K+ Current in Hippocampal Pyramidal Neurons
Martin Stocker, Michael Krause and Paola Pedarzani
Proceedings of the National Academy of Sciences of the United States of America
Vol. 96, No. 8 (Apr. 13, 1999), pp. 4662-4667
Published by: National Academy of Sciences
Stable URL: http://www.jstor.org/stable/47623
Page Count: 6
You can always find the topics here!Topics: Neurons, Electric current, Pyramidal cells, Pharmacology, Neuroscience, Action potentials, In situ hybridization, Kinetics, Brain, Signals
Were these topics helpful?See something inaccurate? Let us know!
Select the topics that are inaccurate.
Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
Preview not available
In hippocampal and other cortical neurons, action potentials are followed by afterhyperpolarizations (AHPs) generated by the activation of small-conductance Ca2+-activated K+ channels (SK channels). By shaping the neuronal firing pattern, these AHPs contribute to the regulation of excitability and to the encoding function of neurons. Here we report that CA1 pyramidal neurons express an AHP current that is suppressed by apamin and is involved in the control of repetitive firing. This current presents distinct kinetic and pharmacological features, and it is modulated differently than the apamin-insensitive slow AHP current. Furthermore, our in situ hybridizations show that the apamin-sensitive SK subunits are expressed in CA1 pyramidal neurons, providing a potential molecular correlate to the apamin-sensitive AHP current. Altogether, these results clarify the discrepancy between the reported high density of apamin-binding sites in the CA1 region and the apparent lack of an apamin-sensitive current in CA1 pyramidal neurons, and they may explain the effects of this toxin on hippocampal synaptic plasticity and learning.
Proceedings of the National Academy of Sciences of the United States of America © 1999 National Academy of Sciences