P/Q-type calcium channels activate neighboring calcium-dependent potassium channels in mouse motor nerve terminals

被引:0
|
作者
Dario A. Protti
Osvaldo D. Uchitel
机构
[1] Instituto de Biología Celular y Neurociencias: ”Pr. Dr. Eduardo P. de Robertis”,
[2] Facultad de Medicina,undefined
[3] Universidad de Buenos Aires,undefined
[4] Paraguay 2155,undefined
[5] Buenos Aires (1121),undefined
[6] Argentina,undefined
[7] Max-Planck-Institut für biophysikalische Chemie,undefined
[8] Am Fassberg,undefined
[9] D-37077 Göttingen,undefined
[10] Germany,undefined
来源
Pflügers Archiv | 1997年 / 434卷
关键词
Key words Neuromuscular junction; Synaptic transmission; Calcium buffers; ω-Agatoxin IVA; FTX; Calcium channels toxins;
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学科分类号
摘要
 The identity of the voltage-dependent calcium channels (VDCC), which trigger the Ca2+-gated K+ currents (IK(Ca)) in mammalian motor nerve terminals, was investigated by means of perineurial recordings. The effects of Ca2+ chelators with different binding kinetics on the activation of IK(Ca) were also examined. The calcium channel blockers of the P/Q family, ω-agatoxin IVA (ω-Aga-IVA) and funnel-web spider toxin (FTX), have been shown to exert a strong blocking effect on IK(Ca). In contrast, nitrendipine and ω-conotoxin GVIA (ω-CgTx) did not affect the Ca2+-activated K+ currents. The intracellular action of the fast Ca2+ buffers BAPTA and DM-BAPTA prevented the activation of the IK(Ca), while the slow Ca2+ buffer EGTA was ineffective at blocking it. These data indicate that P/Q-type VDCC mediate the Ca2+ influx which activates IK(Ca). The spatial association between Ca2+ and Ca2+-gated K+ channels is discussed, on the basis of the differential effects of the fast and slow Ca2+ chelators.
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页码:406 / 412
页数:6
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