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首页> 外文期刊>The European Journal of Neuroscience >Effect of halothane on neuronal excitation in the superficial dorsal horn of rat spinal cord slices: evidence for a presynaptic action.
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Effect of halothane on neuronal excitation in the superficial dorsal horn of rat spinal cord slices: evidence for a presynaptic action.

机译:氟烷对大鼠脊髓片浅背角神经元兴奋的影响:突触前作用的证据。

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The action of the volatile anaesthetic halothane on optically recorded neuronal excitation in juvenile rat spinal cord slices was investigated. Prolonged neuronal excitation lasting approximately 100 ms was evoked in the superficial dorsal horn after single-pulse dorsal root stimulation that activated both A- and C-fibres. Halothane depressed the neuronal excitation in a concentration-dependent manner (IC50 0.21 mm, Imax 28%). In Ca2+-free solution, dorsal root stimulation induced excitation with a short duration of several tens of milliseconds, in which the excitation of the postsynaptic component was largely eliminated. Under these conditions, halothane also depressed the excitation concentration-dependently (IC50 0.46 mm, Imax 60%). Most of the suppression occurred within 5 min of halothane application, and the effect of halothane was fully reversible upon washout of the anaesthetic. Application of bicuculline and strychnine or picrotoxin, or reduction of extracellular Cl- concentration ([Cl-]o), had no effect on halothane inhibition. Applications of K+ channel blockers tetraethyl ammonium, 4-aminopyridine, Cs+ or Ba2+ either had no effect or augmented the inhibitory effect of halothane. On the other hand, the degree of inhibition by halothane was found to be dependent on [K+]o; the higher [K+]o, the larger the depression. In addition, decreases in [Na+]o and [Mg2+]o reduced the excitation similar to that of halothane treatment, and the degree of halothane inhibition became larger with lower [Mg2+]o. These results lead to a hypothesis that halothane suppresses the excitation of presynaptic elements by inhibiting presynaptic Na+ channels by shifting the steady-state inactivation curve in the hyperpolarizing direction.
机译:研究了挥发性麻醉剂氟烷对未成年大鼠脊髓切片中光学记录的神经元兴奋的作用。在单脉冲背根刺激同时激活了A纤维和C纤维后,在浅浅的背角中引起了大约100毫秒的持续神经元兴奋。氟烷以浓度依赖性的方式抑制神经元兴奋(IC50 0.21 mm,Imax 28%)。在无Ca 2+溶液中,背根刺激可在几十毫秒的短时间内引起兴奋,其中很大程度上消除了突触后成分的兴奋。在这些条件下,氟烷也依赖于抑制激发浓度(IC50 0.46 mm,Imax 60%)。大多数抑制作用发生在使用氟烷的5分钟内,并且洗完麻醉剂后氟烷的作用是完全可逆的。施用双小分子和士的宁或微毒素,或降低细胞外Cl-浓度([Cl-] o),对氟烷的抑制没有影响。 K +通道阻滞剂的应用四乙基铵,4-氨基吡啶,Cs +或Ba2 +无效或增强了氟烷的抑制作用。另一方面,发现氟烷的抑制程度取决于[K +] o。 [K +] o越高,凹陷越大。另外,[Na +] o和[Mg2 +] o的减少与氟烷类似,降低了激发,并且[Mg2 +] o越低,氟烷的抑制程度就越大。这些结果导致一个假说,氟烷通过在超极化方向上移动稳态失活曲线来抑制突触前的Na +通道,从而抑制了突触前元素的激发。

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