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首页> 外文期刊>BMC Neuroscience >Isoflurane depresses hippocampal CA1 glutamate nerve terminals without inhibiting fiber volleys
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Isoflurane depresses hippocampal CA1 glutamate nerve terminals without inhibiting fiber volleys

机译：异氟烷可抑制海马CA1谷氨酸神经末梢而不会抑制纤维凌空

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Background Anesthetic-induced CNS depression is thought to involve reduction of glutamate release from nerve terminals. Recent studies suggest that isoflurane reduces glutamate release by block of Na channels. To further investigate this question we examined the actions of isoflurane, TTX, extracellular Ca2+, CNQX and stimulus voltage (stim) on glutamate-mediated transmission at hippocampal excitatory synapses. EPSPs were recorded from CA1 neurons in rat hippocampal brain slices in response to Schaffer-collateral fiber stimulation. Results Isoflurane (350 μM; 1 MAC) reversibly depressed EPSP amplitudes by ~60% while facilitation increased ~20%. Consistent with previous studies, these results indicate a presynaptic site of action that involves reduced excitation-release coupling. EPSPs were depressed to comparable levels by TTX (60 nM) or lowered stim, but facilitation was not changed, indicating a simple failure of axonal conduction. Similarly, partial antagonism of postsynaptic glutamate receptors with CNQX (10 μM) depressed EPSP amplitudes with no change in facilitation. However, EPSP depression by low external Ca2+ (0.8 mM) was accompanied by an increase in facilitation comparable to isoflurane. Isoflurane depression of EPSP amplitudes could also be partly reversed by high external Ca2+ (4 mM) that also decreased facilitation. Isoflurane or low Ca2+ markedly reduced the slopes of fiber volley (FV)-EPSP input-output curves, consistent with little or no effect on FVs. By contrast, TTX didn't alter the FV-EPSP curve slope, indicating that EPSP depression resulted from FV depression. FVs were remarkably resistant to isoflurane. Somatic spike currents were unaffected by 350 μM (1 MAC) isoflurane as well. The EC50 for isoflurane depression of FVs was ~2.8 mM (12 vol. %; 8 MAC). Conclusion Isoflurane appears to depress CA1 synapses at presynaptic sites downstream from Na channels, as evident by the increased facilitation that accompanies EPSP depression. Fiber volleys did not exhibit depression by isoflurane, as has been reported for other brain regions.
机译：背景技术麻醉药引起的中枢神经系统抑制被认为可减少谷氨酸从神经末梢的释放。最近的研究表明，异氟烷可通过阻断Na通道来减少谷氨酸的释放。为了进一步研究这个问题，我们研究了异氟烷，TTX，细胞外Ca 2 + ，CNQX和刺激电压（刺激）对谷氨酸介导的海马兴奋性突触传递的作用。响应于Schaffer附带纤维刺激，从大鼠海马脑片CA1神经元中记录到EPSP。结果异氟烷（350μM; 1 MAC）可逆地将EPSP幅度降低了约60％，而促进作用则提高了约20％。与以前的研究一致，这些结果表明突触前的作用部位涉及减少的兴奋释放耦合。 TTX（60 nM）或降低的刺激将EPSP压低至可比较的水平，但促进作用没有改变，表明轴突传导简单失败。同样，CNQX（10μM）对突触后谷氨酸受体的部分拮抗作用使EPSP幅度降低，而促进作用没有改变。然而，低外部Ca 2 + （0.8 mM）引起的EPSP降低伴随着与异氟烷相当的促进作用的增加。较高的外部Ca 2 + （4 mM）也可以部分逆转EPSP振幅的异氟烷降低，这也降低了促进作用。异氟烷或低Ca 2 + 显着降低了纤维齐射（FV）-EPSP输入-输出曲线的斜率，对FV几乎没有影响。相比之下，TTX并没有改变FV-EPSP曲线的斜率，表明EPSP下降是由FV下降引起的。 FV对异氟烷具有显着的抗性。体细胞尖峰电流也不受350μM（1 MAC）异氟烷的影响。 FV异氟醚抑制的EC 50 为〜2.8 mM（12％（体积）; 8 MAC）。结论异氟烷似乎可以抑制Na通道下游突触前位点的CA1突触，这可通过EPSP抑郁症的促进作用增强来证明。正如其他大脑区域所报道的那样，纤维齐射没有显示出异氟烷引起的抑郁。

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