The regulation of intracellular pH by identified glial cells and neurones in the central nervous system of the leech.
The regulation of intracellular pH by identified glial cells and neurones in the central nervous system of the leech.
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水蛭中枢神经系统中已鉴定的神经胶质细胞和神经元对细胞内 pH 值的调节。
DOI：
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发表时间：
1987
期刊：
影响因子：
--
通讯作者：
W. Schlue
中科院分区：
文献类型：
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作者：
J. W. Deitmer;W. Schlue
1.使用双管中性载体pH敏感微电极测量细胞内pH（pHi）和神经堆胶质细胞（n.g.）细胞和已鉴定的水蛭水蛭神经元。2. H+在n.g.发现细胞和神经元中的电不平衡。n.g.的平均pHi。细胞为6.87 ± 0.13（平均值± S.D.）。HEPES缓冲水蛭盐水（pHo = 7.4）中的平均值（n = 27）和2% CO2 - 11 mM-HCO 3（-）-盐水中的平均值（n = 13）。在HEPES缓冲水蛭盐水中，Retzius神经元的平均pHi为7.28 +/-0.1（n = 20），在有害神经元中为7.32 +/-0.15（n = 12），在2% CO2 - 11 mM-HCO 3（-）缓冲盐水中为7.20 +/-0.15（n = 10）和7.27 +/-0.16（n = 6），分别3.根据水蛭生理盐水中从2% CO2 - 11 mM-HCO 3-变为5% CO2 - 22 mM-HCO 3-后的pHi变化计算，细胞质缓冲能力为20 - 30 mM/pH单位（n.g.）。细胞和12和33 mM/pH单位之间的神经元。4. n.g.中pHi的回收率细胞从实验诱导的酸化（添加和去除20 mM-NH 4Cl）依赖于外部Na+的存在。与使用的缓冲系统无关，当外部Na+被N-甲基-D-葡糖胺交换时，pHi恢复受到抑制。阿米洛利（2 - 3 mM）使这些n.g.中的pHi恢复速率降低约50%。细胞5.在无CO2-HCO 3（-）-的盐水中，或在存在阴离子交换阻滞剂4-乙酰氨基-4 '-异硫氰基芪-2，2'-二磺酸（SITS，0.5 mM）的情况下，在n.g.细胞这表明HCO 3（-）依赖性膜转运对ngpHi调节有显着贡献细胞6.当HEPES缓冲盐水被2% CO2 - 11 mM-HCO 3（-）缓冲盐水替换时，n.g.细胞增加了0.31个pH单位。这种碱性转变在去除CO2-HCO 3-后是可逆的，并且在无Na+-盐水中不存在。1 mM-呋塞米或0.5 mM-SITS均不抑制该作用。（400字处截断摘要）
1. Double‐barrelled, neutral‐carrier pH‐sensitive micro‐electrodes were used to measure the intracellular pH (pHi) and the pHi regulation of neuropile glial (n.g.) cells and of identified neurones of the leech Hirudo medicinalis. 2. The distribution of H+ in the n.g. cells and in the neurones was found not to be in electrical equilibrium. The mean pHi of the n.g. cells was 6.87 +/‐ 0.13 (mean +/‐ S.D. of mean here and for all following data n = 27) in HEPES‐buffered leech saline (pHo = 7.4) and 7.18 +/‐ 0.19 (n = 13) in 2% CO2‐11 mM‐HCO3(‐)‐saline. The mean pHi was 7.28 +/‐ 0.1 (n = 20) in Retzius neurones and 7.32 +/‐ 0.15 (n = 12) in noxious neurones in HEPES‐buffered leech saline, and 7.20 +/‐ 0.15 (n = 10) and 7.27 +/‐ 0.16 (n = 6) in 2% CO2‐11 mM‐HCO3(‐)‐buffered saline in these two types of neurones, respectively. 3. The cytoplasmic buffering power, as calculated by the change in pHi following the change from 2% CO2‐11 mM‐HCO3‐ to 5% CO2‐22 mM‐HCO3‐ in the leech saline, was 20‐30 mM/pH unit in the n.g. cells and between 12 and 33 mM/pH unit in the neurones. 4. The recovery of pHi in n.g. cells from an experimentally induced acidification (addition and removal of 20 mM‐NH4Cl) was dependent on the presence of external Na+. Independent of the buffer system used, pHi recovery was inhibited when external Na+ was exchanged by N‐methyl‐D‐glucamine. Amiloride (2‐3 mM) reduced the rate of pHi recovery by about 50% in these n.g. cells. 5. In CO2‐HCO3(‐)‐free saline, or in the presence of the anion exchange blocker 4‐acetamido‐4'‐isothiocyanostilbene‐2, 2'‐disulphonic acid (SITS, 0.5 mM), pHi recovery from an acid load was often slowed by up to 50% in n.g. cells. This suggests that there is a significant contribution of a HCO3(‐)‐dependent membrane transport to pHi regulation in n.g. cells. 6. When a HEPES‐buffered saline was exchanged by a 2% CO2‐11 mM‐HCO3(‐)‐buffered saline, the pHi of n.g. cells increased by 0.31 pH units. This alkaline shift was reversible upon removal of the CO2‐HCO3‐ and was absent in the Na+‐free saline. It was not inhibited by 1 mM‐furosemide or by 0.5 mM‐SITS.(ABSTRACT TRUNCATED AT 400 WORDS)
影响因子：
2.5
作者：
KRAIG, RP;FERREIRAFILHO, CR;NICHOLSON, C
通讯作者：
NICHOLSON, C