Domestic crickets (Acheta domesticus) as an animal model to study Parkinson's disease

Abstract

Impaired glutamatergic neurotransmission and neuronal metabolic dysfunction are classic alterations in the pathophysiology of Parkinson's disease (PD). The substantia nigra compacta of the brain (the area where the primary pathological lesion is located) is particularly exposed to oxidative stress and metabolic damage. A reduced ability to cope with metabolic demands, possibly related to impaired mitochondrial function, may make the substantia nigra highly vulnerable to the effects of glutamate, which acts as a neurotoxin in the presence of impaired cellular energy metabolism. Taking into account that insects and mammals share a similar molecular architecture in terms of brain function, this work investigated whether domestic crickets (Acheta domesticus) can be used as an animal model for the study of PD. For this, the crickets received an intra‐lymphatic injection (between the second and third tergit of the ventral abdominal segment) of glutamate (10 µl; 2M). Control animals received a similar volume of PBS solution. Twenty‐four hours after treatment, the brains of the animals were dissected. We use our oxygraph‐2K system (OROBOROS Instruments) to determine mitochondrial respiration by activating mitochondrial complexes (CI, CII, CI&II, and CIV) and the production of reactive oxygen species (ROS). Our preliminary results showed that glutamate treatment significantly reduced the respiration of mitochondrial complexes CI, CII, and CI&II, even though the activity of complex IV (an indicator of the number of mitochondria) was not reduced between treatments. On the other hand, mitochondrial production of reactive oxygen species (ROS) in glutamate‐treated animals was significantly increased when both mitochondrial complexes I&II were active, but this pattern was reversed when only one of the complexes I or II was active. Because similar alterations have been observed in the brains of mammals with Parkinson's disease, these results strongly suggest that domestic crickets can be used as an animal model to investigate the mitochondrial mechanisms involved in this disease.