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首页> 外文期刊>IBRO Reports >Effects of subanesthetic intravenous ketamine infusion on neuroplasticity-related proteins in the prefrontal cortex, amygdala, and hippocampus of Sprague-Dawley rats
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Effects of subanesthetic intravenous ketamine infusion on neuroplasticity-related proteins in the prefrontal cortex, amygdala, and hippocampus of Sprague-Dawley rats

机译:麻醉下氯胺酮静注对Sprague-Dawley大鼠前额叶皮层,杏仁核和海马神经可塑性相关蛋白的影响

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摘要

Ketamine, a multimodal dissociative anesthetic, is a powerful analgesic administered following trauma due to its hemodynamic and respiratory stability. However, ketamine can cause hallucination and dissociation which may adversely impact traumatic memory after an injury. The effects of ketamine on proteins implicated in neural plasticity are unclear due to different doses, routes, and timing of drug administration in previous studies. Here, we investigated the effects of a single intravenous (IV) ketamine infusion on protein levels in three brain regions of rats. Adult male Sprague-Dawley rats with indwelling IV catheters underwent an auditory fear conditioning (three pairings of tone and mild footshock 0.8?mA, 0.5?s) and received a high dose of IV ketamine (0 or 40?mg/kg/2?h) infusion (Experiment 1). In a follow-up study, animals received a low dose of IV ketamine (0 or 10?mg/kg/2?h) infusion (Experiment 2). Two hours after the infusion, brain tissue from the medial prefrontal cortex (mPFC), hippocampus, and amygdala were collected for western blot analyses. Protein levels of a transcription factor (c-Fos), brain-derived neurotrophic factor (BDNF), and phosphorylated extracellular signal-regulated kinase (pERK) were quantified in these regions. The 40?mg/kg ketamine infusion increased c-Fos levels in the mPFC and amygdala as well as pERK levels in the mPFC and hippocampus. The 10?mg/kg ketamine infusion increased BDNF levels in the amygdala, but decreased pERK levels in the mPFC and hippocampus. These findings suggest that a clinically relevant route of ketamine administration produces dose-dependent and brain region-specific effects on proteins involved in neuroplasticity.
机译:氯胺酮是一种多模式的解离性麻醉剂,由于其血液动力学和呼吸稳定性,是一种在创伤后给予的强大镇痛药。但是,氯胺酮会引起幻觉和解离,这可能会对受伤后的创伤记忆产生不利影响。氯胺酮对牵涉神经可塑性的蛋白质的影响尚不清楚,原因是先前研究中药物的剂量,途径和给药时间不同。在这里,我们调查了单次静脉内(IV)氯胺酮输注对大鼠三个大脑区域蛋白质水平的影响。成年雄性Sprague-Dawley大鼠在留置静脉导管的情况下进行了听觉恐惧调节(三对语气和轻微的足震0.8?mA,0.5?s),并接受了大剂量的IV氯胺酮(0或40?mg / kg / 2?)。 h)输液(实验1)。在一项后续研究中,动物接受了低剂量的氯胺酮静脉输注(0或10?mg / kg / 2?h)(实验2)。输注两小时后,收集来自内侧前额叶皮层(mPFC),海马和杏仁核的脑组织用于Western印迹分析。在这些区域中定量了转录因子(c-Fos),脑源性神经营养因子(BDNF)和磷酸化的细胞外信号调节激酶(pERK)的蛋白质水平。氯胺酮的40?mg / kg输注增加了mPFC和杏仁核中的c-Fos水平,以及mPFC和海马中的pERK水平。 10?mg / kg氯胺酮输注可增加杏仁核中的BDNF水平,但降低mPFC和海马中的pERK水平。这些发现表明,氯胺酮的临床相关给药途径对涉及神经可塑性的蛋白质产生剂量依赖性和脑区域特异性作用。

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