RAPIDLY ACTIVATING HYDROGEN-ION CURRENTS IN PERFUSED NEURONS OF THE SNAIL, LYMNAEA-STAGNALIS
RAPIDLY ACTIVATING HYDROGEN-ION CURRENTS IN PERFUSED NEURONS OF THE SNAIL, LYMNAEA-STAGNALIS
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DOI：
10.1113/jphysiol.1984.sp015241
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发表时间：
1984-01-01
影响因子：
5.5
通讯作者：
MOODY, W
中科院分区：
文献类型：
--
作者：
BYERLY, L;MEECH, R;MOODY, W
从田螺食道周围神经环中提取细胞。用含有天冬氨酸Cs、EGTA [乙二醇-双（β-氨基乙基醚）-N，N“-四乙酸]和pH缓冲液。在正电位下观察到时间依赖性、电压依赖性的残余外向电流。它们主要由H+携带。高内部pH值、低外部pH值、外部Cd 2+和4-氨基吡啶都会降低外向H+电流。外部四乙基铵离子减少H+电流，但在这些细胞中的K+电流有更有效的阻断作用。所有5个代理商降低最大H+电导。此外，Cd 2+，低的外部pH值和高的内部pH值被发现转移的H+电流的电压依赖性更积极的电位。在内部pCa 2+约为7的情况下记录的H+电流与内部pCa 2+接近5的情况下记录的H+电流之间没有显著差异。这里描述的H+通道很可能为托马斯和米奇描述的去极化HSPs神经元中H+渗透性增加提供了基础。根据它们对不同拮抗剂的敏感性判断，H+通道不同于任何其他先前描述的通道，因为它们对质子具有高度选择性。它们在软体动物神经元中的作用可能是补偿由动作电位序列产生的快速细胞内酸化。
Cells from the circumesophageal nerve ring of the pond snail L. stagnalis were internally perfused with solutions containing Cs aspartate, EGTA [ethyleneglycol-bis(.beta.-aminoethylether)-N,N''-tetraacetic acid] and pH buffers. Time-dependent, voltage-dependent residual outward currents were observed at positive potentials. They were carried largely by H+. The outward H+ currents were reduced by high internal pH, low external pH, external Cd2+ and 4-aminopyridine. External tetraethylammonium ions reduced the H+ currents but had a more effective blocking action on the K+ currents in these cells. All 5 agents reduced the maximum H+ conductance. In addition Cd2+, low external pH and high internal pH were found to shift the voltage dependence of the H+ current to more positive potentials. There was no significant difference between H+ currents recorded with the internal pCa2+ about 7 and those recorded with the internal pCa2+ near 5. It is likely that the H+ channel described here provides the basis for the increase in H+ permeability described by Thomas and Meech in depolarized Helix neurons. As judged by their sensitivity to different antagonists, H+ channels are unlike any other previously described channel in that they are highly selective for protons. Their role in molluscan neurons may be to compensate for the rapid intracellular acidification which is generated by trains of action potentials.