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Evidence of Oropharyngeal Dysfunction in Feeding in the Rat Rotenone Model of Parkinsons Disease

机译:帕金森病大鼠鱼藤酮模型中饲喂口咽功能障碍的证据

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摘要

Swallowing disorders in Parkinson's disease are not responsive to dopamine depletion therapy and contribute to morbidity. They are poorly understood owing to a lack of adequate models. We present the first evidence of oropharyngeal changes in a rotenone toxicity model of Parkinson's disease. Rats were recorded while feeding before and after daily rotenone injections at two different doses (2.75 mg/kg and 3 mg/kg). The higher dose had a much more severe parkinsonian phenotype than the low dose. Timing and amplitude of chewing changed, as did the coordination of chewing and swallowing. Dose-dependent effects were evident. These preliminary results indicate that future research in toxicological models of Parkinson's disease should incorporate the study of oropharyngeal dysfunction. A better understanding of nongenetic models of Parkinson's disease in feeding may open new avenues for research into the neurological and behavioral bases for swallowing dysfunction in Parkinson's disease.
机译:帕金森氏症的吞咽障碍对多巴胺耗竭疗法无反应,并导致发病。由于缺乏适当的模型,因此对它们的了解很少。我们提出帕金森氏病鱼藤酮毒性模型中口咽变化的第一个证据。在每天注射鱼藤酮之前和之后以两种不同剂量(2.75μg/ kg和3μmg/ kg)进食时记录大鼠。高剂量的帕金森病表型比低剂量的帕金森病严重得多。咀嚼的时间和幅度以及咀嚼和吞咽的协调性也发生了变化。剂量依赖性作用是明显的。这些初步结果表明,未来对帕金森氏病毒理学模型的研究应纳入对口咽功能障碍的研究。对喂养中帕金森氏病非遗传模型的更好理解可能为研究帕金森氏病吞咽功能障碍的神经学和行为学基础开辟新的途径。

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