...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Archives of Toxicology >Sensorimotor deficits and increased brain nicotinic acetylcholine receptors following exposure to chlorpyrifos and/or nicotine in rats.
【24h】

Sensorimotor deficits and increased brain nicotinic acetylcholine receptors following exposure to chlorpyrifos and/or nicotine in rats.

机译：暴露于毒死rif和/或尼古丁后，大鼠感觉运动功能减退和大脑烟碱型乙酰胆碱受体增加。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Despite well-known adverse effects associated with cigarette smoking, approximately 20% of the US population continues to smoke and many more are exposed to environmental tobacco smoke. Many of the same individuals are also exposed to environmental neurotoxic chemicals such as the organophosphorus insecticide chlorpyrifos. In the present study, the effects of exposure to low doses of nicotine and chlorpyrifos alone and in combination, were studied on the central cholinergic system and sensorimotor performance in rats. Male Sprague-Dawley rats (250-300 g) were treated with nicotine (1 mg/kg s.c., in normal saline), chlorpyrifos (0.1 mg/kg dermally, in 0.1 ml 70% ethanol), or a combination of both, daily for 30 days. Control rats were treated with saline and dermally with ethanol. Sensorimotor behavior was evaluated 24 h following the last dose using a battery of tests. There was a significant deficit in incline plane performance, beam-walk score and beam-walk time following exposure to each chemical, alone or in combination. The deficit in incline plane performance was greater when the two chemicals were given in combination than with either compound alone. Biochemical analysis showed a decrease in cerebellar and an increase in midbrain acetylcholinesterase (AChE) activity following combined exposure. Exposure to nicotine alone resulted in a significant increase in AChE activity in brainstem and midbrain, whereas there was no significant change after exposure to chlorpyrifos, alone. A significant increase in ligand binding to nicotinic acetylcholine receptors (nAChR) was observed in brainstem and cortex following exposure to nicotine or chlorpyrifos. This was further augmented with combined exposure, which caused a modest but significant increase in m2 muscarinic acetylcholine receptors (m2-mAChR) ligand binding in the cortex. These data suggest that exposure to either nicotine or chlorpyrifos or a combination of the two may impair neurobehavioral performance and affect the central nervous system cholinergic pathways.
机译：尽管众所周知，吸烟会带来不利影响，但约有20％的美国人口仍在吸烟，而更多的人则暴露于环境烟草烟雾中。许多相同的个体也暴露于环境神经毒性化学物质，例如有机磷杀虫剂毒死rif。在本研究中，研究了低剂量尼古丁和毒死rif单独使用或联合使用对大鼠中枢胆碱能系统和感觉运动性能的影响。每天用尼古丁（1 mg / kg sc，在生理盐水中），毒死rif（0.1 mg / kg皮肤，在0.1 ml 70％乙醇中）或两者的组合治疗雄性Sprague-Dawley大鼠（250-300 g） 30天。对照大鼠用盐水治疗，并用乙醇皮肤治疗。在最后一次给药后24小时，使用一系列测试评估感觉运动行为。单独或组合使用每种化学品后，斜面性能，束走得分和束走时间均存在明显不足。当两种化学药品组合使用时，倾斜平面性能的缺陷要比单独使用任何一种化合物都要大。生化分析表明，合并暴露后小脑减少，中脑乙酰胆碱酯酶（AChE）活性增加。单独暴露于尼古丁会导致脑干和中脑的AChE活性显着增加，而单独暴露于毒死rif后则没有显着变化。暴露于尼古丁或毒死rif后，在脑干和皮质中观察到配体与烟碱乙酰胆碱受体（nAChR）的结合显着增加。联合暴露进一步增加了暴露，这导致皮质中m2毒蕈碱型乙酰胆碱受体（m2-mAChR）配体结合适度但显着增加。这些数据表明，暴露于尼古丁或毒死or或两者的组合可能会损害神经行为表现并影响中枢神经系统胆碱能途径。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号