Neuron-specific toxicity of chronic acrylamide exposure in C. elegans

Abstract

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.

Keywords: Caenorhabditis elegans; Cholinergic; Dopaminergic; GABAergic; Neurodegeneration; Oxidative stress.