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首页> 外文期刊>Pharmacology, Biochemistry and Behavior >Effect of MK-801 and ketamine on hydroxyl radical generation in the posterior cingulate and retrosplenial cortex of free-moving mice, as determined by in vivo microdialysis.
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Effect of MK-801 and ketamine on hydroxyl radical generation in the posterior cingulate and retrosplenial cortex of free-moving mice, as determined by in vivo microdialysis.

机译：通过体内微透析测定，MK-801和氯胺酮对自由移动小鼠后扣带回和脾后皮质的羟自由基生成的影响。

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摘要

This study investigated the effect of MK-801 and ketamine, N-methyl-D-aspartate (NMDA) receptor antagonists which can induce schizophrenic symptoms and have neurotoxicity in human and animals, on hydroxyl radical (*OH) generation in the posterior cingulate and retrosplenial (PC/RS) cortex of free-moving mice using the salicylic acid trapping technique. MK-801 (0.6 mg/kg) or ketamine (50 mg/kg) acute administration significantly increased *OH levels in mouse PC/RS cortex. The basal *OH levels after MK-801 and ketamine administrations for 7 consecutive days were significantly increased compared with the naive basal levels. MK-801 (0.6 mg/kg) or ketamine (50 mg/kg) challenge after chronic administration further significantly increased dialysate levels of *OH. Our study also found that the release of *OH was secondary to stereotyped behavior, and the intensity of stereotyped behavior induced by MK-801 was more than that induced by ketamine. The results suggested that NMDA receptor antagonists participate in the generation of *OH in the PC/RS cortex of mouse, and oxidative stress, derived from the formation of free radicals, might play an important role in the pathophysiology of these two models of schizophrenia.
机译：这项研究调查了MK-801和氯胺酮，N-甲基-D-天冬氨酸（NMDA）受体拮抗剂（它们可诱导精神分裂症症状并对人和动物具有神经毒性）对后扣带和后肢羟基自由基（* OH）生成的影响。使用水杨酸捕获技术的自由移动小鼠的脾后（PC / RS）皮质。急性施用MK-801（0.6 mg / kg）或氯胺酮（50 mg / kg）可以显着提高小鼠PC / RS皮质的* OH水平。与未使用的基础水平相比，连续7天服用MK-801和氯胺酮后的基础* OH水平显着增加。长期给药后，MK-801（0.6 mg / kg）或氯胺酮（50 mg / kg）激发进一步显着提高* OH的透析液水平。我们的研究还发现，* OH的释放是继定型行为之后的，而MK-801诱导的定型行为的强度大于氯胺酮诱导的定型行为的强度。结果表明，NMDA受体拮抗剂参与了小鼠PC / RS皮层中* OH的生成，而源自自由基形成的氧化应激可能在这两种精神分裂症模型的病理生理中起重要作用。

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