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首页> 外文期刊>Toxicology: An International Journal Concerned with the Effects of Chemicals on Living Systems >Assessment of general anaesthetic cytotoxicity in murine cortical neurones in dissociated culture.
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Assessment of general anaesthetic cytotoxicity in murine cortical neurones in dissociated culture.

机译：分离培养的鼠皮质神经元中的全身麻醉细胞毒性评估。

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摘要

General anaesthetics are proposed to cause unconsciousness by modulating neuronal excitability in the mammalian brain through mechanisms that include enhancement of inhibitory GABA(A) receptor currents and suppression of excitatory glutamate receptor responses. Both intravenous and volatile agents may produce neurotoxic effects during early postnatal rodent brain development through similar mechanisms. In the following study, we investigated anaesthetic cytotoxicity in primary cortical neurones and glia from postnatal day 2-8 mice. Cultures at 4-20 days in vitro were exposed to combinations of ketamine (100 muM to 3 mM), nitrous oxide (75%, v/v) and/or isoflurane (1.5-5%, v/v) for 6-12 h. Neuronal survival and cell death were measured via microtubule associated protein 2 immunoassay and lactate dehydrogenase release assays, respectively. Clinically relevant anaesthetic concentrations of ketamine, nitrous oxide and isoflurane had no significant neurotoxic effects individually or when given as anaesthetic cocktails, even with up to 12 h exposure. This lack of neurotoxicity was observed regardless of whether cultures were prepared from postnatal day 0-2 or day 8 mice, and was also unaffected by number of days in vitro (DIV 4-20). Significant neurotoxic effects were only observed at supraclinical concentrations (e.g. 1-3 mM ketamine). Our study suggests that neurotoxicity previously reported in vivo is not due to direct cytotoxicity of anaesthetic agents, but results from other impacts of the anaesthetised state during early brain development.
机译：提议使用全身麻醉剂通过包括增强抑制性GABA（A）受体电流和抑制兴奋性谷氨酸受体反应的机制来调节哺乳动物大脑中神经元的兴奋性，从而引起意识丧失。静脉和挥发性药物在产后啮齿动物早期大脑发育过程中都可能通过类似的机制产生神经毒性作用。在以下研究中，我们调查了出生后第2-8天的小鼠在原代皮层神经元和神经胶质细胞中的麻醉细胞毒性。将体外4-20天的培养物暴露于氯胺酮（100μM至3 mM），一氧化二氮（75％，v / v）和/或异氟烷（1.5-5％，v / v）的组合中6-12 H。神经元存活和细胞死亡分别通过微管相关蛋白2免疫测定和乳酸脱氢酶释放测定来测量。氯胺酮，一氧化二氮和异氟烷的临床相关麻醉剂浓度单独或以麻醉混合物的形式使用时，即使暴露长达12小时也没有明显的神经毒性作用。无论是从出生后第0-2天还是从第8天小鼠制备培养物，都观察到这种神经毒性缺乏，并且不受体外天数的影响（DIV 4-20）。仅在超临床浓度（例如1-3 mM氯胺酮）下才能观察到明显的神经毒性作用。我们的研究表明，先前在体内报道的神经毒性不是由于麻醉剂的直接细胞毒性，而是由于早期大脑发育过程中麻醉状态的其他影响所致。

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