Extracellular alkaline-acid-alkaline transients in the rat spinal cord evoked by peripheral stimulation
Extracellular alkaline-acid-alkaline transients in the rat spinal cord evoked by peripheral stimulation
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外周刺激引起的大鼠脊髓细胞外碱-酸-碱瞬变
DOI：
10.1016/0006-8993(90)90625-l
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发表时间：
1990
期刊：
影响因子：
2.9
通讯作者：
J. Svoboda
中科院分区：
文献类型：
--
作者：
Eva Sykova´;J. Svoboda
采用双筒pH敏感微电极研究了未受刺激的大鼠脊髓细胞外pH值的区域差异。下背角（板层III-VII）中的pH值约为7.15，即比脑脊液中测量的pH值低约0.2个pH单位。当对后爪施加急性伤害性刺激（捏、按、热）时，发现pHeby0.01 - 0.05pH单位的瞬时酸变化。通过皮下注射姜黄素或在后爪上应用1-3 ml热油引起的化学或热损伤使下背角的pH基线长期下降约0.05-0.1 pH单位。伤后2-10 min pH值开始下降，持续2 h以上。神经电刺激（10-100 Hz，20-60 s）引起pH值的双相（酸-碱）或三相（碱-酸-碱）变化，其深度分布与同时记录的[K+]e的增加相似。初始碱移约0.005 pH单位，发现显着降低镧3+，H+通道阻滞剂。乙酰唑胺（碳酸酐酶抑制剂）加速并增加了约0.1-0.2 pH单位的主要酸位移，表明细胞外液的高缓冲能力可能会阻碍酸扰动的解决。刺激诱发的酸位移被阿米洛利、SITS、DIDS和La 3+阻断，因此具有复杂的机制，包括Na+/H+交换、Cl−/HCO 3 −共转运和/或Na+/Cl−/H+/HCO 3 −反向转运以及通过电压敏感性H+通道的H+流出。后刺激碱性移位（碱性下冲）被哇巴因阻断，反映了K+和H+的主动运输过程的耦合清除。
Regional differences in extracellular pH (pHe) were found in unstimulated rat spinal cord using double-barrel pH-sensitive microelectrodes. The pHein the lower dorsal horn (laminae III–VII) was about 7.15, i.e. by about 0.2 pH units lower than the measured in the cerebrospinal fluid. Transient acid shifts in pHeby 0.01–0.05 pH units were found when acute nociceptive stimuli (pinch, press, heat) were applied to the hind paw. Chemical or thermal injury evoked by subcutaneous injection of turpentine or by application of 1–3 ml of hot oil onto the hindpaw produced a long-term decrease in pHebase line in the lower dorsal horn by about 0.05–0.1 pH units. The decrease in pHebegan 2–10 min after injury and persisted for more than 2 h. Electrical nerve stimulation (10–100 Hz, 20–60 s) elicited biphasic (acid-alkaline) or triphasic (alkaline-acid-alkaline) changes in pHewhich have a similar depth profile as the concomitantly recorded increase in [K+]e. An initial alkaline shift by about 0.005 pH units was found to be significantly decreased by La3+, an H+channel blocker. The dominating acid shift by about 0.1–0.2 pH units was accelerated and increased by acetazolamide (carbonic anhydrase inhibitor) showing that the high buffering capacity of the extracellular fluid may hamper the resolution of acid perturbations. Stimulation-evoked acid shifts were blocked by amiloride, SITS, DIDS and La3+and therefore have a complex mechanism which includes Na+/H+exchange, Cl−/HCO3−cotransport and/or Na+/Cl−/H+/HCO3−antiport and H+efflux through voltage-sensitive H+channels. The poststimulation alkaline shift (alkaline undershoot) was blocked by ouabain and reflects coupled clearance of K+and H+by active transport processes.
影响因子：
2.5
作者：
KRAIG, RP;FERREIRAFILHO, CR;NICHOLSON, C
通讯作者：
NICHOLSON, C
影响因子：
5.5
作者：
BALESTRINO, M;SOMJEN, GG
通讯作者：
SOMJEN, GG