Action of Isoflurane on the Substantia Gelatinosa Neurons of the Adult Rat Spinal Cord
Action of Isoflurane on the Substantia Gelatinosa Neurons of the Adult Rat Spinal Cord
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DOI：
10.1097/00000542-200502000-00021
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发表时间：
2005-02
期刊：
影响因子：
8.8
通讯作者：
A. Wakai;T. Kohno;T. Yamakura;M. Okamoto;T. Ataka;H. Baba
中科院分区：
文献类型：
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作者：
A. Wakai;T. Kohno;T. Yamakura;M. Okamoto;T. Ataka;H. Baba
背景：尽管异氟烷是一种挥发性麻醉剂，可以阻断对有害刺激（不动和镇痛）的运动反应并抑制自主反应，但它如何在脊髓神经元水平上发挥这些作用尚不完全清楚。方法：使用全细胞膜片钳技术，在成年大鼠脊髓切片的第 II 层神经元中检查异氟烷的临床相关浓度（1 只大鼠最低肺泡浓度 [MAC]）对电诱发和自发兴奋/抑制传递以及对外源给予 β-氨基丁酸 A 型受体激动剂蝇蕈醇的反应的影响。还检查了异氟烷对动作电位产生膜特性的影响。结果：沐浴应用的异氟烷（1.5%，1只大鼠MAC）减少了背根诱发的多突触电流，但不减少单突触的兴奋性突触后电流。谷氨酸微型兴奋性突触后电流也不受异氟醚的影响。相反，异氟烷延长了诱发的和微型氨基丁酸A型受体介导的抑制性突触后电流的衰减阶段，并增加了蝇蕈醇诱导的电流的幅度。异氟烷对动作电位放电活性影响不大。结论：异氟烷增强γ-氨基丁酸介导的抑制性传递，导致脊髓背角神经元兴奋性降低。这可能是异氟烷在脊髓中发挥抗伤害作用的可能机制。
Background:Although isoflurane, a volatile anesthetic, can block the motor response to noxious stimulation (immobility and analgesia) and suppress autonomic responsiveness, how it exerts these effects at the neuronal level in the spinal cord is not fully understood. Methods:The effects of a clinically relevant concentration (1 rat minimum alveolar concentration [MAC]) of isoflurane on electrically evoked and spontaneous excitatory/inhibitory transmission and on the response to exogenous administration of the -aminobutyric acid type A receptor agonist muscimol were examined in lamina II neurons of adult rat spinal cord slices using the whole cell patch clamp technique. The effect of isoflurane on the action potential–generating membrane property was also examined. Results:Bath-applied isoflurane (1.5%, 1 rat MAC) diminished dorsal root–evoked polysynaptic but not monosynaptic excitatory postsynaptic currents. Glutamatergic miniature excitatory postsynaptic currents were also unaffected by isoflurane. In contrast, isoflurane prolonged the decay phase of evoked and miniature -aminobutyric acid type A receptor–mediated inhibitory postsynaptic currents and increased the amplitude of the muscimol-induced current. Isoflurane had little effect on action potential discharge activity. Conclusions:Isoflurane augments -aminobutyric acid–mediated inhibitory transmission, leading to a decrease in the excitability of spinal dorsal horn neurons. This may be a possible mechanism for the antinociceptive effect of isoflurane in the spinal cord.