Opioid receptor-mediated inhibition of omega-conotoxin GVIA-sensitive calcium channel currents in rat intracardiac neurons.
Opioid receptor-mediated inhibition of omega-conotoxin GVIA-sensitive calcium channel currents in rat intracardiac neurons.
复制标题
阿片受体介导的大鼠心内神经元 omega-芋螺毒素 GVIA 敏感钙通道电流的抑制。
DOI：
10.1152/jn.1998.79.2.753
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发表时间：
1998
影响因子：
2.5
通讯作者：
Trequattrini,C
中科院分区：
文献类型：
--
作者：
Adams,DJ;Trequattrini,C
Adams, David J. and Carlo Trequattrini.Opioid receptor-mediated inhibition of ω-conotoxin GVIA-sensitive calcium channel currents in rat intracardiac neurons.J. Neurophysiol.79: 753–762, 1998. Modulation of depolarization-activated ionic conductances by opioid receptor agonists was investigated in isolated parasympathetic neurons from neonatal rat intracardiac ganglia by using the whole cell perforated patch clamp technique. Met-enkephalin (10 μM) altered the action potential waveform, reducing the maximum amplitude and slowing the rate of rise and repolarization but the afterhyperpolarization was not appreciably altered. Under voltage clamp, 10 μM Met-enkephalin selectively and reversibly inhibited the peak amplitude of high-voltage–activated Ca2+channel currents elicited at 0 mV by ∼52% and increased three- to fourfold the time to peak. Met-enkephalin had no effect on the voltage dependence of steady-state inactivation but shifted the voltage dependence of activation to more positive membrane potentials whereby stronger depolarization was required to open Ca2+channels. Half-maximal inhibition of Ba2+current (IBa) amplitude was obtained with 270 nM Met-enkephalin or Leu-enkephalin. The opioid receptor subtype selective agonists, DAMGO and DADLE, but not DPDPE, inhibitedIBaand were antagonized by the opioid receptor antagonists, naloxone and naltrindole with IC50s of 84 nM and 1 μM, respectively. The κ-opioid receptor agonists, bremazocine and dynorphin A, did not affect Ca2+channel current amplitude or kinetics. Taken together, these data suggest that enkephalin-induced inhibition of Ca2+channels in rat intracardiac neurons is mediated primarily by the μ-opioid receptor type. Addition of Met-enkephalin after exposure to 300 nM ω-conotoxin GVIA, which blocked ∼75% of the total Ca2+channel current, failed to cause a further decrease of the residual current. Met-enkephalin inhibited the ω-conotoxin GVIA-sensitive but not the ω-conotoxin-insensitiveIBain rat intracardiac neurons. Dialysis of the cell with a GTP-free intracellular solution or preincubation of the neurons in Pertussis toxin (PTX) abolished the attenuation ofIBaby Met-enkephalin, suggesting the involvement of a PTX-sensitive Gprotein in the signal transduction pathway. The activation of μ-opioid receptors and subsequent inhibition of N-type Ca2+channels in the soma and terminals of postganglionic intracardiac neurons is likely to inhibit the release of ACh and thereby regulate vagal transmission to the mammalian heart.
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μ-阿片受体介导的 N 型钙通道电流抑制
DOI：
--
发表时间：
1991
期刊：
Proceedings of the Royal Society of London. Series B: Biological Sciences
影响因子：
--
作者：
E. Seward;C. Hammond;G. Henderson
通讯作者：
G. Henderson
心脏前脑啡肽原 mRNA 的翻译和培养心肌细胞脑啡肽肽的分泌。
DOI：
10.1152/ajpheart.1992.263.5.h1560
发表时间：
1992
期刊：
The American journal of physiology
影响因子：
--
作者：
Springhorn,JP;Claycomb,WC
通讯作者：
Claycomb,WC
豚鼠心脏副交感神经、交感神经和感觉神经中的内源性阿片肽
影响因子：
3.6
作者：
P. Steele;E. Aromataris;B. Riederer
通讯作者：
B. Riederer
刺激心室肌细胞上的阿片受体可降低 L 型 Ca2 通道电流。
影响因子：
5
作者：
R. Xiao;H. Spurgeon;M. Capogrossi;E. Lakatta
通讯作者：
E. Lakatta
豚鼠心脏自主神经的调节肽（SP、NT、VIP、PHI、ENK）。
DOI：
--
发表时间：
1984
期刊：
Clinical and Experimental Hypertension Part A Theory and Practice
影响因子：
--
作者：
M. Reinecke;W. Forssmann
通讯作者：
W. Forssmann