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首页> 外文期刊>Pharmacology, Biochemistry and Behavior >Behavioral deficits and cellular damage following developmental ethanol exposure in rats are attenuated by CP-101,606, an NMDAR antagonist with unique NR2B specificity
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Behavioral deficits and cellular damage following developmental ethanol exposure in rats are attenuated by CP-101,606, an NMDAR antagonist with unique NR2B specificity

机译：CP-101,606是一种具有独特NR2B特异性的NMDAR拮抗剂，可减轻大鼠发育性乙醇暴露后的行为缺陷和细胞损伤。

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NMDAR-mediated excitotoxicity has been implicated in some of the impairments following fetal ethanol exposure. Previous studies suggest that both neuronal cell death and some of the behavioral deficits can be reduced by NMDAR antagonism during withdrawal, including antagonism of a subpopulation of receptors containing NR2B subunits. To further investigate NR2B involvement, we selected a compound, CP-101,606 (CP) which binds selectively to NR2B/2B stoichiometries, for both in vitro and in vivo analyses. For the in vitro study, hippocampal explants were exposed to ethanol for 10 days and then 24 h following removal of ethanol, cellular damage was quantified via propidium iodide fluorescence. In vitro ethanol withdrawal-associated neurotoxicity was prevented by CP (10 and 25 nM). In vivo ethanol exposure was administered on PNDs 1-7 with CP administered 21 h following cessation. Activity (PNDs 20-21), motor skills (PNDs 31-33), and maze navigation (PNDs 43-44) were all susceptible to ethanol insu treatment with CP (15 mg/kg) rescued these deficits. Our findings show that CP-101,606, a drug that blocks the NR2B/2B receptor, can reduce some of the damaging effects of "3rd trimester" alcohol exposure in our rodent model. Further work is clearly warranted on the neuroprotective potential of this drug in the developing brain.
机译：NMDAR介导的兴奋性毒性与胎儿乙醇暴露后的某些损伤有关。先前的研究表明，戒断期间NMDAR拮抗作用（包括对含有NR2B亚基的受体亚群的拮抗作用）可以减少神经元细胞死亡和某些行为缺陷。为了进一步研究NR2B的参与，我们选择了一种化合物CP-101,606（CP），该化合物可选择性地与NR2B / 2B的化学计量结合，用于体内和体外分析。对于体外研究，将海马外植体暴露于乙醇中10天，然后在除去乙醇后24小时，通过碘化丙啶荧光定量细胞损伤。 CP（10和25 nM）可以防止体外乙醇戒断相关的神经毒性。在PND 1-7上给予体内乙醇暴露，在停止后21小时给予CP。活动（PND 20-21），运动技能（PND 31-33）和迷宫导航（PND 43-44）都容易受到乙醇的侵害。 CP（15 mg / kg）治疗挽救了这些不足。我们的发现表明，在我们的啮齿动物模型中，阻断NR2B / 2B受体的药物CP-101,606可以减少“第三孕期”酒精暴露的某些破坏作用。显然需要对该药物在发育中的脑中的神经保护潜力进行进一步的研究。

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