IK1 channels do not contribute to the slow afterhyperpolarization in pyramidal neurons

Kang Wang, Pedro Mateos-Aparicio, Christoph Hönigsperger, Vijeta Raghuram, Wendy W. Wu, Margreet C. Ridder, Pankaj Sah, Jim Maylie, Johan F. Storm, John P. Adelman

Research output: Contribution to journalArticlepeer-review

21 Scopus citations


In pyramidal neurons such as hippocampal area CA1 and basolateral amygdala, a slow afterhyperpolarization (sAHP) follows a burst of action potentials, which is a powerful regulator of neuronal excitability. The sAHP amplitude increases with aging and may underlie age related memory decline. The sAHP is due to a Ca2+-dependent, voltage-independent K+ conductance, the molecular identity of which has remained elusive until a recent report suggested the Ca2+-activated K+ channel, IK1 (KCNN4) as the sAHP channel in CA1 pyramidal neurons. The signature pharmacology of IK1, blockade by TRAM-34, was reported for the sAHP and underlying current. We have examined the sAHP and find no evidence that TRAM-34 affects either the current underling the sAHP or excitability of CA1 or basolateral amygdala pyramidal neurons. In addition, CA1 pyramidal neurons from IK1 null mice exhibit a characteristic sAHP current. Our results indicate that IK1 channels do not mediate the sAHP in pyramidal neurons.

Original languageEnglish (US)
Article numbere11206
Issue numberJANUARY2016
StatePublished - Jan 14 2016

ASJC Scopus subject areas

  • Neuroscience(all)
  • Immunology and Microbiology(all)
  • Biochemistry, Genetics and Molecular Biology(all)


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