Cav1.2 calcium channels modulate the spiking pattern of hippocampal pyramidal cells

被引:26
作者
Lacinova, Lubica [1 ]
Moosmang, Sven [2 ]
Langwieser, Nicole [2 ]
Hofmann, Franz [2 ]
Kleppisch, Thomas [2 ]
机构
[1] Slovak Acad Sci, Inst Mol Physiol & Genet, Bratislava 83334, Slovakia
[2] Tech Univ Munich, Inst Pharmakol & Toxikol, D-80802 Munich, Germany
关键词
neuronal excitability; action potential; repetitive firing; CA1 pyramidal cells; Ca(v)1.2 channel;
D O I
10.1016/j.lfs.2007.10.009
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Ca(v)1.2 L-type calcium channels support hippocampal synaptic plasticity, likely by facilitating dendritic Ca2+ influx evoked by action potentials (AP) back-propagated from the soma. Ca2+ influx into hippocampal neurons during somatic AN is sufficient to activate signalling pathways associated with late phase LTP. Thus, mechanisms controlling AP firing of hippocampal neurons are of major functional relevance. We examined the excitability of CA1 pyramidal cells using somatic current-clamp recordings in brain slices from control type mice and mice with the Ca(v)1.2 gene inactivated in principal hippocampal neurons. Lack of the Ca(v)1.2 protein did not affect either affect basic characteristics, such as resting membrane potential and input resistance, or parameters of single action potentials (AP) induced by 5 ms depolarising current pulses. However, CA1 hippocampal neurons from control and mutant mice differed in their patterns of AP firing during 500 ms depolarising current pulses: threshold voltage for repetitive firing was shifted significantly by about 5 mV to more depolarised potentials in the mutant mice (p<0.01), and the latency until firing of the first AP was prolonged (73.2 +/- 6.6 ms versus 48.1 +/- 7.8 ms in control; p < 0.05). CA1 pyramidal cells from the mutant mice also showed a lowered initial spiking frequency within an AP train. In control cells, isradipine had matching effects, while BayK 8644 facilitated spiking. Our data demonstrate that Ca(v)1.2 channels are involved in regulating the intrinsic excitability of CA1 pyramidal neurons. This cellular mechanism may contribute to the known function of Ca(v)1.2 channels in supporting synaptic plasticity and memory. (C) 2007 Elsevier Inc. All rights reserved.
引用
收藏
页码:41 / 49
页数:9
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