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首页> 外文期刊>The European Journal of Neuroscience >Actions of propofol on substantia gelatinosa neurones in rat spinal cord revealed by in vitro and in vivo patch-clamp recordings.
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Actions of propofol on substantia gelatinosa neurones in rat spinal cord revealed by in vitro and in vivo patch-clamp recordings.

机译：体外和体内膜片钳记录揭示了异丙酚对大鼠脊髓中明胶神经元神经元的作用。

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Propofol, an intravenous general anaesthetic, exerts anaesthetic actions through interaction with gamma-aminobutyric acid type A (GABA(A)) receptors in the supraspinal nervous system. However, whether propofol has any significant effects on synaptic transmission at the spinal level and whether it exhibits antinociceptive action is still not fully clarified. Spontaneous activity and stimulus-evoked responses of substantia gelatinosa (SG) neurones to noxious pinch stimuli were recorded using spontaneously breathing rats under propofol anaesthesia using in vivo whole-cell patch-clamp techniques. Precise actions of propofol on GABAergic and glycinergic inhibitory postsynaptic currents (IPSCs) as well as excitatory postsynaptic currents (EPSCs) in SG neurones were also analyzed in spinal cord slice preparations. At clinical doses (5 mg/kg), propofol reversibly depressed action potentials elicited by noxious mechanical stimuli applied to the skin in the majority (6/8) of SG neurons recorded under in vivo conditions. This depression may have been caused by interactions of propofol with GABA(A) receptors, as decay time of GABAergic sIPSCs was prolonged after propofol injection (128 +/- 11% of control, n = 5) with minimal effect on EPSCs. Although prolongation of IPSCs in vivo was reversible, IPSCs were progressively prolonged even after washout of propofol when the effect was tested using spinal cord slices. Propofol had a mild depressant effect on Adelta- and C-afferent-mediated EPSCs. We conclude that systemic bolus injection of propofol reversibly depressed nociceptive transmission, at least in part, by enhancing postsynaptic GABA(A) receptor-mediated responses in the SG.
机译：丙泊酚，一种静脉内麻醉剂，通过与脊髓上神经系统中的A型γ-氨基丁酸（GABA（A））受体相互作用而发挥麻醉作用。然而，异丙酚是否在脊髓水平上对突触传递有任何显着影响以及它是否显示出抗伤害感受的作用仍未完全弄清楚。使用体内全细胞膜片钳技术，在异丙酚麻醉下自发呼吸的大鼠，记录明胶（SG）神经元对有害捏刺激的自发活动和刺激诱发的反应。在脊髓切片制剂中，还分析了异丙酚对SG神经元中GABA能和甘氨酸抑制性突触后电流（IPSC）以及兴奋性突触后电流（EPSC）的精确作用。在临床剂量（5 mg / kg）下，在体内条件下记录的大部分（6/8）SG神经元中，对皮肤施加有害的机械刺激后，异丙酚可逆地降低了其动作电位。这种抑郁症可能是由于丙泊酚与GABA（A）受体的相互作用引起的，因为丙泊酚注射后GABA能sIPSCs的衰变时间延长了（对照组的128 +/- 11％，n = 5），对EPSC的影响最小。尽管体内IPSCs的延长是可逆的，但是当使用脊髓切片测试效果时，甚至在异丙酚被冲洗后，IPSCs也会逐渐延长。丙泊酚对Adelta和C-afferent介导的EPSC具有轻度的抑制作用。我们得出的结论是，至少部分通过增强SG中的突触后GABA（A）受体介导的反应，全身推注异丙酚可逆地抑制了伤害性传递。

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