IKCa Channels Are a Critical Determinant of the Slow AHP in CA1 Pyramidal Neurons

被引:74
作者
King, Brian [1 ]
Rizwan, Arsalan P. [1 ]
Asmara, Hadhimulya [1 ]
Heath, Norman C. [1 ]
Engbers, Jordan D. T. [1 ]
Dykstra, Steven [1 ]
Bartoletti, Theodore M. [1 ]
Hameed, Shahid [1 ]
Zamponi, Gerald W. [1 ]
Turner, Ray W. [1 ]
机构
[1] Univ Calgary, Hotchkiss Brain Inst, Calgary, AB T2N 4N1, Canada
基金
加拿大健康研究院;
关键词
ACTIVATED POTASSIUM CHANNELS; RAT HIPPOCAMPAL-NEURONS; CA2+-ACTIVATED K+ CHANNELS; SMALL-CONDUCTANCE; AFTERHYPERPOLARIZATION; CELLS; MODULATION; INHIBITOR; BINDING; KCA3.1;
D O I
10.1016/j.celrep.2015.03.026
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Control over the frequency and pattern of neuronal spike discharge depends on Ca2+-gated K+ channels that reduce cell excitability by hyperpolarizing the membrane potential. The Ca2+-dependent slow afterhyperpolarization (sAHP) is one of the most prominent inhibitory responses in the brain, with sAHP amplitude linked to a host of circuit and behavioral functions, yet the channel that underlies the sAHP has defied identification for decades. Here, we show that intermediate-conductance Ca2+-dependent K+ (IKCa) channels underlie the sAHP generated by trains of synaptic input or postsynaptic stimuli in CA1 hippocampal pyramidal cells. These findings are significant in providing a molecular identity for the sAHP of central neurons that will identify pharmacological tools capable of potentially modifying the several behavioral or disease states associated with the sAHP.
引用
收藏
页码:175 / 182
页数:8
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