Pharmacological characterization of Na+ influx via voltage-gated Na+ channels in spinal cord astrocytes.
Pharmacological characterization of Na+ influx via voltage-gated Na+ channels in spinal cord astrocytes.
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脊髓星形胶质细胞中通过电压门控钠离子通道钠离子流入的药理学特征。
DOI：
10.1152/jn.1997.78.6.3249
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发表时间：
1997
期刊：
影响因子：
--
通讯作者：
Waxman,SG
中科院分区：
文献类型：
--
作者：
Rose,CR;Ransom,BR;Waxman,SG
罗斯，克莉丝汀R.，布鲁斯河Ransom和Stephan G. Waxman.脊髓星形胶质细胞中通过电压门控Na+通道的Na+内流的药理学表征.神经生理学杂志78：3249-3258，1997.脊髓星形胶质细胞显示高密度的电压门控Na+通道。为了研究Na+通过这些通道流入对培养的脊髓星形胶质细胞中Na+稳态的贡献，我们用荧光染料钠结合苯并呋喃三乙酸酯测量细胞内Na+浓度（[Na+]i）。星状和非星状星形胶质细胞，显示Na+电流具有不同的属性，进行了分化。这些细胞中的基线[Na+] i为8.5 mM，100 μM河豚毒素（TTX）未改变。用藜芦碱（100 μM）抑制Na+通道失活，在44%的星状星形胶质细胞和64%的非星状星形胶质细胞中引起[Na+] i增加47.1 mM和9.7 mM。约30%的细胞与藜芦碱反应，[Na+]减少约1.2mM，乌头碱引起类似的[Na+]变化。乌藨子苷的作用可被TTX阻断，被（α-）蝎毒素放大，且通常是可逆的。藜芦碱诱导的[Na+] i增加在细胞外[K+]升高的膜去极化后减少。在用4-氨基吡啶阻断K+通道的过程中，[Na+] i恢复到基线水平不变。[Na+] TTX不改变离子型非N-甲基-d-天冬氨酸受体激动剂红藻氨酸盐引起的增加。我们的结果表明，Na+通过电压门控Na+通道的内流不是静息状态下脊髓星形胶质细胞中胶质细胞Na+，K+-ATP酶活性的先决条件，也不参与红藻氨酸引起的[Na+] i增加。然而，在Na+通道失活的药理学抑制过程中，Na+通道可以作为Na+内流的主要途径，并介导[Na+]i的大扰动，这表明Na+通道失活在这些细胞中起着重要的功能作用。
Rose, Christine R., Bruce R. Ransom, and Stephan G. Waxman.Pharmacological characterization of Na+influx via voltage-gated Na+channels in spinal cord astrocytes.J. Neurophysiol.78: 3249–3258, 1997. Spinal cord astrocytes display a high density of voltage-gated Na+channels. To study the contribution of Na+influx via these channels to Na+homeostasis in cultured spinal cord astrocytes, we measured intracellular Na+concentration ([Na+]i) with the fluorescent dye sodium-binding benzofuran isophthalate. Stellate and nonstellate astrocytes, which display Na+currents with different properties, were differentiated. Baseline [Na+]iwas 8.5 mM in these cells and was not altered by 100 μM tetrodotoxin (TTX). Inhibition of Na+channel inactivation by veratridine (100 μM) evoked a [Na+]iincrease of 47.1 mM in 44% of stellate and 9.7 mM in 64% of nonstellate astrocytes. About 30% of cells reacted to veratridine with a [Na+]idecrease of ∼2 mM. Qualitatively similar [Na+]ichanges were caused by aconitine. The effects of veratridine were blocked by TTX, amplified by (α-)scorpion toxin and usually were readily reversible. Veratridine-induced [Na+]iincreases were reduced upon membrane depolarization with elevated extracellular [K+]. Recovery to baseline [Na+]iwas unaltered during blocking of K+channels with 4-aminopyridine. [Na+]iincreases evoked by the ionotropic non-N-methyl-d-aspartate receptor agonist kainate were not altered by TTX. Our results indicate that influx of Na+via voltage- gated Na+channels is not a prerequisite for glial Na+,K+-ATPase activity in spinal cord astrocytes at rest nor does it seem to be involved in [Na+]iincreases evoked by kainate. During pharmacological inhibition of Na+channel inactivation, however, Na+channels can serve as prominent pathways of Na+influx and mediate large perturbations in [Na+]i, suggesting that Na+channel inactivation plays an important functional role in these cells.
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体外脊髓星形胶质细胞的离子通道。
影响因子：
2.5
作者：
C. Thio;S. Waxman;H. Sontheimer
通讯作者：
H. Sontheimer
影响因子：
2.5
作者：
SONTHEIMER, H;WAXMAN, SG
通讯作者：
WAXMAN, SG
DOI：
10.1073/pnas.87.24.9833
发表时间：
1990-12-01
影响因子：
11.1
作者：
SONTHEIMER, H;MINTURN, JE;RANSOM, BR
通讯作者：
RANSOM, BR
脂溶性毒素被认为对 Na 通道具有特异性，可阻断神经元细胞中的 Ca2 通道
影响因子：
64.8
作者：
G. Romey;M. Lazdunski
通讯作者：
M. Lazdunski
培养的大鼠海马神经元细胞内钠的调节。
DOI：
10.1113/jphysiol.1997.sp021951
发表时间：
1997
期刊：
The Journal of physiology
影响因子：
--
作者：
Rose,CR;Ransom,BR
通讯作者：
Ransom,BR