Comparison of Neurobehavioral Changes in Mice Treated with Mitochondrial Toxins—Rotenone and MPTP

Time Course of Neurobehavioral Disruptions and Regional Brain Metabolism Changes in the Rotenone Mice Model of Parkinson’s Disease

“…Our previous work on the topic, comparing the neurotoxicity of rotenone to that of MPTP, had shown the faster progression of PD-like symptoms and SNpc neurodegeneration, but without the decrease in dopamine in basal ganglia, characteristic to PD [ 24 ]. However, we used the outbred CD-1 mice strain, which may have significantly affected our findings.…”

“…The status of lipid peroxidation (LPO) and endogenous antioxidant system in the brainstem homogenized tissue samples were studied using Fe 2+ -induced chemiluminescence (CL) analysis in accordance with the protocol used in our previous work [ 24 ]. As in previous works, we analyzed the following reaction parameters: h, mV—rapid initial burst of CL corresponding to the level of preformed LPO products; T,c—latent period prior to further substrate oxidation, reflecting the endogenous antioxidant potential.…”

“…In our previous work with the same rotenone model [ 18 ], we have shown that the rotenone metabolic effect in the brains of mice is less specific than that of rats, disrupting COX activity not only in the SN, but also in various cortical structures [ 23 ]. The comparison of rotenone chronic exposure to CD-1 mice with exposure to another toxin, MPTP, showed faster dynamics of motor symptoms evolution in the rotenone model, but they lacked the specific neuropathological changes that are characteristic of PD [ 24 ]. However, the question of whether these effects would be reproduced in the C57BL/6 mice strain, which is more frequently used in PD research, remained open.…”