Sasaki Rika, Hirota Koki, Roth Sheldon H, Yamazaki Mitsuaki
Department of Anesthesiology, Toyama Medical and Pharmaceutical University School of Medicine, Toyama, Japan.
Anesthesiology. 2002 Mar;96(3):681-7. doi: 10.1097/00000542-200203000-00026.
Magnesium ion (Mg2+) is involved in important processes as modulation of ion channels, receptors, neurotransmitter release, and cell excitability in the central nervous system. Although extracellular Mg2+ concentration ([Mg2+]o) can be altered during general anesthesia, there has been no evidence for [Mg2+]o-dependent modification of anesthetic actions on neural excitability in central nervous system preparations. The purpose of current study was to determine whether the effects of volatile anesthetics are [Mg2+]o-dependent in mammalian central nervous system.
Extracellular electrophysiologic recordings from CA1 neurons in rat hippocampal slices were used to investigate the effects of [Mg2+]o and anesthetics on population spike amplitude and excitatory postsynaptic potential slope.
The depression of population spike amplitudes and excitatory postsynaptic potential slopes by volatile anesthetics were significantly dependent on [Mg2+]o. The effects were attenuated in the presence of a constant [Mg2+]o/extracellular Ca2+ concentration ratio. However, neither N-methyl-d-aspartate receptor antagonists nor a non-N-methyl-d-aspartate receptor antagonist altered the [Mg2+]o-dependent anesthetic-induced depression of population spikes. Volatile anesthetics produced minimal effects on input-output (excitatory postsynaptic potential-population spike) relations or the threshold for population spike generation. The effects were not modified by changes in [Mg2+]o. In addition, the population spike amplitudes, elicited via antidromic (nonsynaptic) stimulation, were not influenced by [Mg2+]o in the presence of volatile anesthetics.
These results provide support that alteration of [Mg2+]o modifies the actions of volatile anesthetics on synaptic transmission and that the effects could be, at least in part, a result of presynaptic Ca2+ channel-related mechanisms.
镁离子（Mg2+）参与重要过程，如调节离子通道、受体、神经递质释放以及中枢神经系统中的细胞兴奋性。尽管在全身麻醉期间细胞外Mg2+浓度（[Mg2+]o）可能会改变，但尚无证据表明在中枢神经系统制剂中，[Mg2+]o依赖性地改变麻醉药对神经兴奋性的作用。本研究的目的是确定挥发性麻醉药的作用是否在哺乳动物中枢神经系统中依赖于[Mg2+]o。
使用大鼠海马切片中CA1神经元的细胞外电生理记录来研究[Mg2+]o和麻醉药对群体峰电位幅度和兴奋性突触后电位斜率的影响。
挥发性麻醉药对群体峰电位幅度和兴奋性突触后电位斜率的抑制作用显著依赖于[Mg2+]o。在恒定的[Mg2+]o/细胞外Ca2+浓度比存在时，这些作用减弱。然而，N-甲基-D-天冬氨酸受体拮抗剂和非N-甲基-D-天冬氨酸受体拮抗剂均未改变[Mg2+]o依赖性麻醉药诱导的群体峰电位抑制。挥发性麻醉药对输入-输出（兴奋性突触后电位-群体峰电位）关系或群体峰电位产生阈值的影响最小。这些作用不受[Mg2+]o变化的影响。此外，在存在挥发性麻醉药的情况下，通过逆向（非突触）刺激引发的群体峰电位幅度不受[Mg2+]o的影响。
这些结果支持[Mg2+]o的改变会改变挥发性麻醉药对突触传递的作用，并且这些作用至少部分可能是突触前Ca2+通道相关机制的结果。
