不同温度下大鼠海马切片中酸中毒及缺氧引起的顺向反应阻断

Acidosis and blockade of orthodromic responses caused by anoxia in rat hippocampal slices at different temperatures.

作者信息

Krnjević K, Walz W

机构信息

Anaesthesia Research Department, McGill University, Montréal, Québec, Canada.

出版信息

J Physiol. 1990 Mar;422:127-44. doi: 10.1113/jphysiol.1990.sp017976.

DOI:10.1113/jphysiol.1990.sp017976

PMID:2352175

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1190124/

Abstract

Interstitial pH (pHo) and field responses (to stratum radiatum stimulation) were recorded simultaneously with double-barrelled microelectrodes in the CA1 region of hippocampal slices from Sprague-Dawley rats. 2. Both the relative acidity and amplitude of field responses increased with depth, reaching a maximum near the centre of the slice. When the temperature was raised from 22 to 37 degrees C, this pHo gradient was greater than 2 times steeper, but the field responses were much diminished. 3. Standard anoxic tests (substituting 95% N2 + 5% CO2 for 95% O2 + 5% CO2, for 2 min) tended to reduce pHo and population spikes, but these effects were highly temperature sensitive: at approximately 22 degrees C the blocking rate was only 12.3 +/- 4.6% and delta pHo -0.018 +/- 0.0157 units, both per minute; corresponding changes at 34-35 degrees C were 67.6 +/- 11.9% and -0.065 +/- 0.0046 units per minute. Highly significant linear correlations between rates of block and delta pHo gave a mean slope of 90.4 +/- 17.6% per 0.1 unit of acid change. 4. Anoxia caused similar temperature-dependent increases in acidity in stratum pyramidale and radiatum, but in the latter field responses (EPSPs) were much less depressed after 2 min of anoxia. 5. When slices were superfused with acid medium (low [HCO3-]), much greater reductions in pHo were needed to depress responses, giving a mean slope of 17.7% per 0.1 pH unit. 6. In glucose-free medium, there was a slow alkaline shift in pHo (0.13 +/- 0.036 units); population spikes and the acid transients evoked by anoxia disappeared. 7. It was concluded that acidosis cannot be the immediate cause of the similar depressions of postsynaptic excitability seen during anoxia and hypoglycaemia. 8. In further tests, DL-p-hydroxyphenyl-lactic acid, a blocker of lactate transport, failed to diminish acid transients evoked by anoxia, indicating that these are not mediated principally by lactate transport.

摘要

使用双管微电极在来自Sprague-Dawley大鼠的海马切片CA1区同时记录间质pH（pHo）和场反应（对辐射层刺激）。2. 场反应的相对酸度和幅度均随深度增加，在切片中心附近达到最大值。当温度从22℃升至37℃时，这种pHo梯度陡度增加超过2倍，但场反应大大减弱。3. 标准缺氧试验（用95%N₂ + 5%CO₂替代95%O₂ + 5%CO₂，持续2分钟）倾向于降低pHo和群体峰电位，但这些效应对温度高度敏感：在约22℃时，阻断率仅为12.3±4.6%，pHo每分钟变化-0.018±0.0157单位；在34 - 35℃时，相应变化为每分钟67.6±11.9%和-0.065±0.0046单位。阻断率与pHo变化率之间存在高度显著的线性相关性，酸变化每0.1单位的平均斜率为90.4±17.6%。4. 缺氧在锥体细胞层和辐射层引起类似的温度依赖性酸度增加，但在后者，缺氧2分钟后场反应（兴奋性突触后电位）的抑制程度要小得多。5. 当切片用酸性介质（低[HCO₃⁻]）灌流时，需要更大程度地降低pHo才能抑制反应，每0.1 pH单位的平均斜率为17.7%。6. 在无糖培养基中，pHo有缓慢的碱化变化（0.13±0.036单位）；群体峰电位和缺氧诱发的酸瞬变消失。7. 得出的结论是，酸中毒不可能是缺氧和低血糖期间突触后兴奋性类似抑制的直接原因。8. 在进一步的试验中，乳酸转运阻滞剂DL - 对羟基苯乳酸未能减少缺氧诱发的酸瞬变，表明这些瞬变主要不是由乳酸转运介导的。