Sources of Ca2+ for different Ca2+-activated K+ conductances in neurones of the rat superior cervical ganglion
Sources of Ca2+ for different Ca2+-activated K+ conductances in neurones of the rat superior cervical ganglion
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DOI：
10.1113/jphysiol.1996.sp021599
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发表时间：
1996-09-01
影响因子：
5.5
通讯作者：
McLachlan, EM
中科院分区：
文献类型：
--
作者：
Davies, PJ;Ireland, DR;McLachlan, EM
1．采用细胞内记录和单电极电压钳技术，研究了体外分离的年轻成年大鼠颈上神经节神经元中各种Ca2+激活的K+电导的作用。2．用Co2+（2 mM）替代Ca2+或添加Cd2+（100 μM）后，动作电位幅度和半宽度增加或减少（在不同细胞中），但后超极化（AHP）和超阈值电压阶跃后的外向尾电流均显着减弱（约75％）。 3．添加卡雷布毒素(60 nM)或硝苯地平(10 μM)增加了动作电位半宽度(约25％)，但对AHP或尾电流没有显着影响。4．添加 apamin (100 nM) 或 omega-芋螺毒素 GVIA (100 nM) 会降低 AHP 和尾电流（约 60%），但不会显着影响动作电位。 50% 神经元中存在的 AHP 的长期 apamin 抗性成分被 ryanodine (20 mu M) 阻断。5。 omega-芋螺毒素 MVIIC (150 nM) 和 omega-agatoxin IVA (200 nM) 对动作电位半宽度或 AHP 没有显着影响。6。 Ca2+通道阻滞剂均不影响AHP和尾电流的延长兰尼碱敏感成分。7．我们的结论是，在大鼠交感神经元中，Ca2+通过L型通道进入选择性激活大电导Ca2+激活的K+通道（BK型），有助于动作电位复极化，而Ca2+通过N型通道进入选择性激活小电导Ca2+激活K+通道（SK型），有助于AHP。 Ca2+ 进入 R 型 Ca2+ 通道通过激活细胞内储存的 Ca2+ 释放来延长 AHP。
1. The role of various Ca2+-activated K+ conductances were investigated using intracellular recording and single-electrode voltage clamp in neurones of superior cervical ganglia isolated in vitro from young adult rats.2. Following replacement-of Ca2+ with Co2+ (2 mM) or the addition of Cd2+ (100 mu M), action potential amplitude and half-width either increased or decreased (in different cells), but both the after-hyperpolarization (AHP) and the outward tail current following a suprathreshold voltage step were markedly attenuated (by about 75%).3. Addition of charybdotoxin (60 nM) or nifedipine (10 mu M) increased action potential halfwidth (by about 25%) but had no significant effect-on the AHP or tail current.4. Addition of apamin (100 nM) or omega-conotoxin GVIA (100 nM) reduced the AHP and tail current (by about 60%) but did not significantly affect the action potential. A prolonged apamin-resistant component of the AHP present in 50% of neurones was blocked by ryanodine (20 mu M).5. omega-Conotoxin MVIIC (150 nM) and omega-agatoxin IVA (200 nM) had no significant effects on the action potential half-width or the AHP.6. None of the Ca2+ channel blockers affected the prolonged ryanodine-sensitive component of the AHP and tail current.7. We conclude that, in rat sympathetic neurones, Ca2+ entry via L-type channels selectively activates large conductance Ca2+-activated K+ channels (BK type) contributing to action potential repolarization, whereas Ca2+ entry via N-type channels selectively activates small conductance Ca2+-activated K+ channels (SK type) contributing to the AHP. Ca2+ entry sia R-type Ca2+ channels prolongs the AHP by activating Ca2+ release from intracellular stores.