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

ELife
Kang WangJohn P Adelman

Abstract

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 Ca(2+)-dependent, voltage-independent K(+) conductance, the molecular identity of which has remained elusive until a recent report suggested the Ca(2+)-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.

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Citations

Apr 18, 2020·The European Journal of Neuroscience·Cecilia Tubert, Mario Gustavo Murer
Aug 15, 2018·Frontiers in Molecular Neuroscience·Aravind S KshatriTeresa Giraldez
Jul 25, 2019·Annual Review of Pharmacology and Toxicology·Brandon M BrownHeike Wulff
Aug 24, 2019·Neurobiology of Learning and Memory·Amy R Dunn, Catherine C Kaczorowski

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