Histamine promotes excitability in bovine adrenal chromaffin cells by inhibiting an M‐current
Histamine promotes excitability in bovine adrenal chromaffin cells by inhibiting an M‐current
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组胺通过抑制 M 电流促进牛肾上腺嗜铬细胞的兴奋性
DOI：
10.1113/jphysiol.2001.013370
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发表时间：
2002
期刊：
影响因子：
--
通讯作者：
P. Marley
中科院分区：
文献类型：
--
作者：
D. Wallace;Chen Chen;P. Marley
本研究采用穿孔贴片技术研究了组胺对牛肾上腺嗜铬细胞的电生理反应。组胺引起短暂超极化，继而持续去极化7.2±1.4 mV，并伴有自发动作电位频率的增加。用thapsigargin(100 Nm)耗尽细胞内钙库后，超极化被消除，而用apamin(100 Nm)可使超极化降低40%。在组胺诱导的去极化过程中，膜电阻增加了约60%，表明K+通道受到抑制。在保持电位为−30 mV的电压阶跃下，观察到典型的M电流的内向电流弛豫。该电流在−为81.6±1.8 mV时逆转，并被M通道阻断剂利诺匹定(10 0μm)所阻断。在应用组胺时，与持续除极对应的时间记录的M电流的幅度降低了40%。在−15 0~−70 mV范围内未观察到内向电流整流现象，格列本脲(10μm)对静息膜电位和对组胺的反应均无影响。结果表明，牛嗜铬细胞存在M-电流，组胺可抑制该电流，导致膜去极化和动作电位放电增加。这些结果首次证明了组胺受体与激活这些细胞中的电压操纵的钙通道的可能机制。
The current study has investigated the electrophysiological responses evoked by histamine in bovine adrenal chromaffin cells using perforated‐patch techniques. Histamine caused a transient hyperpolarization followed by a sustained depolarization of 7.2 ± 1.4 mV associated with an increase in spontaneous action potential frequency. The hyperpolarization was abolished after depleting intracellular Ca2+ stores with thapsigargin (100 nm), and was reduced by 40 % with apamin (100 nm). Membrane resistance increased by about 60 % during the histamine‐induced depolarization suggesting inhibition of a K+ channel. An inward current relaxation, typical of an M‐current, was observed in response to negative voltage steps from a holding potential of −30 mV. This current reversed at −81.6 ± 1.8 mV and was abolished by the M‐channel inhibitor linopirdine (100 μm). During application of histamine, the amplitude of M‐currents recorded at a time corresponding with the sustained depolarization was reduced by 40 %. No inward current rectification was observed in the range −150 to −70 mV, and glibenclamide (10 μm) had no effect on either resting membrane potential or the response to histamine. The results show that an M‐current is present in bovine chromaffin cells and that this current is inhibited during sustained application of histamine, resulting in membrane depolarization and increased discharge of action potentials. These results demonstrate for the first time a possible mechanism coupling histamine receptors to activation of voltage‐operated Ca2+ channels in these cells.
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DOI：
10.1073/pnas.95.12.7151
发表时间：
1998-06-09
影响因子：
11.1
作者：
Cruzblanca, H;Koh, DS;Hille, B
通讯作者：
Hille, B
影响因子：
56.9
作者：
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通讯作者：
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DOI：
10.1113/jphysiol.1992.sp019343
发表时间：
1992
期刊：
The Journal of physiology
影响因子：
--
作者：
Xu,ZJ;Adams,DJ
通讯作者：
Adams,DJ
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DOI：
10.1113/jphysiol.1985.sp015837
发表时间：
1985
期刊：
The Journal of physiology
影响因子：
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作者：
Sims,SM;Singer,JJ;WalshJr,JV
通讯作者：
WalshJr,JV
DOI：
10.1073/pnas.89.2.554
发表时间：
1992-01-15
影响因子：
11.1
作者：
GELLENS, ME;GEORGE, AL;KALLEN, RG
通讯作者：
KALLEN, RG