Acrylamide is a food-borne chemical with well-known neurotoxic properties. To date, the toxicity mechanisms of chronic acrylamide exposure are not fully understood. Using the genetic model Caenorhabditis elegans, we found that chronic acrylamide exposure induces a locomotor defect that is characterized by severe uncoordination of muscle movement that is distinct from an overall reduction in activity. C. elegans exhibiting chronic acrylamide-induced locomotor defects show significant degeneration to the dopaminergic and cholinergic, but not GABAergic motor neurons. Degeneration of the dopaminergic and cholinergic neurons are found in 58% to 67% of C. elegans after chronic acrylamide exposure, with the varying degrees of severity ranging from neuronal blebbing to complete dendrite loss. The observed pattern of neurotoxicity does not have a heritable effect, as parental exposure to chronic acrylamide does not lead to neurodegeneration in the developed offspring. Overall, these finding illustrate that chronic acrylamide exposure cause locomotor defects by inducing degeneration of specific neuron types in C. elegans.

中文翻译：

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秀丽隐杆线虫慢性丙烯酰胺暴露的神经元特异性毒性。

丙烯酰胺是一种具有众所周知的神经毒性特性的食用化学品。迄今为止，慢性丙烯酰胺暴露的毒性机理尚未完全了解。使用遗传模型秀丽隐杆线虫，我们发现慢性丙烯酰胺暴露会引起运动缺陷，其特征是严重的肌肉运动不协调，与活动的总体减少不同。表现出慢性丙烯酰胺诱导的运动缺陷的秀丽隐杆线虫对多巴胺能和胆碱能表现出明显的变性，但对GABA能运动神经元却没有。慢性丙烯酰胺暴露后，在58％至67％的秀丽隐杆线虫中发现了多巴胺能和胆碱能神经元的变性，其严重程度从神经元起泡到完全树突消失不等。观察到的神经毒性模式没有遗传效应，因为父母暴露于慢性丙烯酰胺不会导致发育后代的神经变性。总体而言，这些发现表明，长期丙烯酰胺暴露会导致秀丽隐杆线虫特定神经元类型的退化，从而引起运动缺陷。