Effects of prenatal ethanol exposure on voltage-dependent calcium entry into neonatal whole brain-dissociated neurons.
Effects of prenatal ethanol exposure on voltage-dependent calcium entry into neonatal whole brain-dissociated neurons.
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产前乙醇暴露对电压依赖性钙进入新生儿全脑游离神经元的影响。
DOI：
10.1111/j.1530-0277.1996.tb05272.x
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
Leslle,SW
中科院分区：
文献类型：
--
作者：
Lee,YH;Spuhler-Phillips,K;Randall,PK;Leslle,SW
研究了产前乙醇暴露对新生儿分离神经元电压依赖性钙离子内流的影响。从产前乙醇处理（ET）、成对喂养（PF）对照和随意（AL）对照组的新生儿中分离的全脑细胞，并加载bra-2。与AL和PF对照治疗相比，产前乙醇暴露导致进入K+去极化细胞的钙离子显著减少。最初，在AL对照动物的解离细胞中，发现硝苯地平（1 μM）、ω-蛇曲霉毒素（100 nM）和ω-芋螺毒素（500 nM）在较小程度上显著抑制45 mM KCl刺激的钙离子内流。为了确定产前乙醇暴露对N-1 P-1和L-型电压依赖性钙通道的抑制作用，在产前乙醇和对照治疗组中分别比较了ω-芋螺毒素、ω-蛇曲霉毒素和硝苯地平的不同组合对新生儿分离神经元的治疗。在存在或不存在单一拮抗剂条件下（ET < AL和PF），产前乙醇暴露对K+刺激的钙内流增加的抑制作用显著降低。乙醇暴露和拮抗剂条件没有明显的相互作用。然而，产前乙醇暴露后钙离子进入减少被双重和三重拮抗剂条件下的更强抑制所取代。ET、PF和AL组之间拮抗剂组合对钙反应抑制的幅度相似。因此，这些结果表明，产前乙醇暴露降低电压依赖性钙进入新生儿分离的神经元的方式，似乎不涉及任何个人的N-，P-，或L-型钙通道的选择性抑制。
The effect of prenatal ethanol exposure on voltage‐dependent calcium entry into neonatal‐dissociated neurons was studied. Dissociated whole brain cells were isolated from neonates of prenatally ethanol‐treated (ET), pair‐fed (PF) control, and ad libitum (AL) control groups and loaded with bra‐2. Prenatal ethanol exposure resulted in a significant reduction of calcium entry into K+‐depolarized cells, compared with AL and PF control treatments. Initially, in dissociated cells from AL control animals, it was found that nifedipine (1 μM), ω‐agatoxin (100 nM), and ω‐conotoxin (500 nM), to a much lesser extent, significantly inhibited the 45 mM KCI‐stimulated calcium entry. To determine the inhibitory action of prenatal ethanol exposure on N‐1P‐1and L‐type voltage‐dependent calcium channels, treatment of neonatal‐dissociated neurons with different combinations of ω‐conotoxin, ω‐agatoxin, and nifedipine, respectively, was compared in the prenatal ethanol and control treatment groups. The inhibition of K+‐stimulated increase in calcium entry by prenatal ethanol exposure was significantly less in the presence or absence of single antagonist conditions (ET < AL and PF). There was no apparent interaction of ethanol exposure and antagonist condition. However, the reduced calcium entry after prenatal ethanol exposure was superseded by the stronger inhibition in dual and triple antagonist conditions. The magnitude of the calcium response inhibition by the antagonist combinations was similar among the ET, PF, and AL groups. Thus, these results suggest that prenatal ethanol exposure decreases voltage‐dependent calcium entry into neonatal‐dissociated neurons in a manner that does not seem to involve the selective inhibition of any individual N‐, P‐, or L‐type calcium channel.