RT Journal Article
SR Electronic
T1 Small Conductance Ca<sup>2+</sup>-Activated K<sup>+</sup> Channel Knock-Out Mice Reveal the Identity of Calcium-Dependent Afterhyperpolarization Currents
JF The Journal of Neuroscience
JO J. Neurosci.
FD Society for Neuroscience
SP 5301
OP 5306
DO 10.1523/JNEUROSCI.0182-04.2004
VO 24
IS 23
A1 Bond, Chris T.
A1 Herson, Paco S.
A1 Strassmaier, Timothy
A1 Hammond, Rebecca
A1 Stackman, Robert
A1 Maylie, James
A1 Adelman, John P.
YR 2004
UL http://www.jneurosci.org/content/24/23/5301.abstract
AB Action potentials in many central neurons are followed by a prolonged afterhyperpolarization (AHP) that influences firing frequency and affects neuronal integration. In hippocampal CA1 pyramidal neurons, the current ascribed to the AHP (IAHP) has three kinetic components. The IfastAHP is predominantly attributable to voltage-dependent K+ channels, whereas Ca2+-dependent and voltage-independent K+channels contribute to the ImediumAHP (ImAHP) and IslowAHP (IsAHP). Apamin, which selectively suppresses a component of the mAHP, increases neuronal excitability and facilitates the induction of synaptic plasticity at Schaffer collateral synapses and hippocampal-dependent learning. The Ca2+-dependent components of the AHP have been attributed to the activity of small conductance Ca2+-activated K+ (SK) channels. Examination of transgenic mice, each lacking one of the three SK channel genes expressed in the CNS, reveals that mice without the SK2 subunit completely lack the apamin-sensitive component of the ImAHP in CA1 neurons, whereas the IsAHP is not different in any of the SK transgenic mice. In each of the transgenic lines, the expression levels of the remaining SK genes are not changed. The results demonstrate that only SK2 channels are necessary for the ImAHP, and none of the SK channels underlie the IsAHP.