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This Article Full Text Full Text (PDF) All Versions of this Article: 585/1/75    most recent jphysiol.2007.138156v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Wallén, P. Articles by Grillner, S. Search for Related Content PubMed PubMed Citation Articles by Wallén, P. Articles by Grillner, S. Related Collections Neuroscience

¹ Nobel Institute for Neurophysiology, Karolinska Institutet, Stockholm, Sweden
² Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden
³ Department Pharmacology & Toxicology, SUNY, Buffalo, NY, USA
⁴ Department of Pharmacology, Yale University School of Medicine, New Haven, CT, USA

The slow afterhyperpolarization (sAHP) following the action potential is the main determinant of spike frequency regulation. The sAHP after single action potentials in neurons of the lamprey locomotor network is largely due to calcium-dependent K⁺ channels (80%), activated by calcium entering the cell during the spike. The residual (20%) component becomes prominent during high level activity (50% of the sAHP). It is not Ca²⁺ dependent, has a reversal potential like that of potassium, and is not affected by chloride injection. It is not due to rapid activation of Na⁺/K⁺-ATPase. This non-K_Ca-sAHP is reduced markedly in amplitude when sodium ions are replaced by lithium ions, and is thus sodium dependent. Quinidine also blocks this sAHP component, further indicating an involvement of sodium-dependent potassium channels (K_Na). Modulators tested do not influence the K_Na-sAHP amplitude. Immunofluorescence labelling with an anti-Slack antibody revealed distinct immunoreactivity of medium-sized and large neurons in the grey matter of the lamprey spinal cord, suggesting the presence of a Slack-like subtype of K_Na channel. The results strongly indicate that a K_Na potassium current contributes importantly to the sAHP and thereby to neuronal frequency regulation during high level burst activity as during locomotion. This is, to our knowledge, the first demonstration of a functional role for the Slack gene in contributing to the slow AHP.

(Received 8 June 2007; accepted after revision 20 September 2007; first published online 20 September 2007)
Corresponding author P. Wallén: Nobel Institute for Neurophysiology, Department of Neuroscience, Karolinska Institutet, SE-171 77 Stockholm, Sweden. Email: peter.wallen{at}ki.se

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