Parent L, Schneider T, Moore C P, Talwar D
Département de Physiologie, Membrane Transport Research Group, Université de Montréal, Montréal, Qué, Canada.
J Membr Biol. 1997 Nov 15;160(2):127-40. doi: 10.1007/s002329900302.
The alpha1 subunit coding for the human brain type E calcium channel (Schneider et al., 1994) was expressed in Xenopus oocytes in the absence, and in combination with auxiliary alpha2delta and beta subunits. alpha1E channels directed with the expression of Ba2+ whole-cell currents that completely inactivated after a 2-sec membrane pulse. Coexpression of alpha1E with alpha2bdelta shifted the peak current by +10 mV but had no significant effect on whole-cell current inactivation. Coexpression of alpha1E with beta2a shifted the peak current relationship by -10 mV, and strongly reduced Ba2+ current inactivation. This slower rate of inactivation explains that a sizable fraction (40 +/- 10%, n = 8) of the Ba2+ current failed to inactivate completely after a 5-sec prepulse. Coinjection with both the cardiac/brain beta2a and the neuronal alpha2bdelta subunits increased by approximately 10-fold whole-cell Ba2+ currents although coinjection with either beta2a or alpha2bdelta alone failed to significantly increase alpha1E peak currents. Coexpression with beta2a and alpha2bdelta yielded Ba2+ currents with inactivation kinetics similar to the beta2a induced currents, indicating that the neuronal alpha2bdelta subunit has little effect on alpha1E inactivation kinetics. The subunit specificity of the changes in current properties were analyzed for all four beta subunit genes. The slower inactivation was unique to alpha1E/beta2a currents. Coexpression with beta1a, beta1b, beta3, and beta4, yielded faster-inactivating Ba2+ currents than currents recorded from the alpha1E subunit alone. Furthermore, alpha1E/alpha2bdelta/beta1a; alpha1E/alpha2bdelta/beta1b; alpha1E/alpha2bdelta/beta3; alpha1E/alpha2bdelta/beta4 channels elicited whole-cell currents with steady-state inactivation curves shifted in the hyperpolarized direction. The beta subunit-induced changes in the properties of alpha1E channel were comparable to modulation effects reported for alpha1C and alpha1A channels with beta3 approximately beta1b > beta1a approximately beta4 >> beta2a inducing fastest to slowest rate of whole-cell inactivation.
编码人脑中E型钙通道的α1亚基（施奈德等人，1994年）在非洲爪蟾卵母细胞中单独表达，以及与辅助α2δ和β亚基共同表达。α1E通道的表达引导了Ba2+全细胞电流，该电流在2秒的膜脉冲后完全失活。α1E与α2βδ共同表达使峰值电流正向移动了10 mV，但对全细胞电流失活没有显著影响。α1E与β2a共同表达使峰值电流关系负向移动了10 mV，并强烈降低了Ba2+电流失活。这种较慢的失活速率解释了在5秒预脉冲后，相当一部分（40±10%，n = 8）的Ba2+电流未能完全失活。与心脏/脑β2a和神经元α2βδ亚基共同注射使全细胞Ba2+电流增加了约10倍，尽管单独与β2a或α2βδ共同注射未能显著增加α1E峰值电流。与β2a和α2βδ共同表达产生的Ba2+电流的失活动力学与β2a诱导的电流相似，表明神经元α2βδ亚基对α1E失活动力学影响很小。对所有四个β亚基基因分析了电流特性变化的亚基特异性。较慢的失活是α1E/β2a电流所特有的。与β1a、β1b、β3和β4共同表达产生的Ba2+电流的失活速度比单独从α1E亚基记录的电流更快。此外，α1E/α2βδ/β1a；α1E/α2βδ/β1b；α1E/α2βδ/β3；α1E/α2βδ/β4通道引发的全细胞电流的稳态失活曲线向超极化方向移动。β亚基诱导的α1E通道特性变化与α1C和α1A通道报道的调节效应相当，其中β3≈β1b＞β1a≈β4＞＞β2a诱导全细胞失活的速度从最快到最慢。
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