Docosahexaenoic acid protection in a rotenone induced Parkinson's model: Prevention of tubulin and synaptophysin loss, but no association with mitochondrial function

Publication date: Available online 19 October 2018Source: Neurochemistry InternationalAuthor(s): Norma Serrano-García, Francisca Fernández-Valverde, Erika Rubi Luis-Garcia, Leticia Granados-Rojas, Tarsila Elizabeth Juárez-Zepeda, Sandra Adela Orozco-Suárez, José Pedraza-Chaverri, Marisol Orozco-Ibarra, Anabel Jiménez-AnguianoAbstractRotenone, a classic mitochondrial complex I inhibitor, leads to dopaminergic neuronal death resulting in a Parkinson's-like-disease. Docosahexaenoic acid (DHA) has shown neuroprotective effects in other experimental models of Parkinson's disease, but its effect on the rotenone-induced parkinsonism is still unknown. We tested whether DHA in vivo exerts a neuroprotective effect on rotenone-induced parkinsonism and explored the mechanisms involved, including mitochondrial function and ultrastructure as well as the expression of tubulin and synaptophysin. We pretreated eighty male Wistar rats with DHA (35 mg/kg/day) for 7 days and then administered rotenone for either 8 or 14 days. We then measured rearing behavior, number of dopaminergic neurons, tyrosine hydroxylase content, tubulin and synaptophysin expression, mitochondrial complex I, respiratory control ratio, mitochondrial transmembrane potential, ATP production activity and mitochondrial ultrastructure. We found that in vivo DHA supply exerted a neuroprotective effect, evidenced by decreased dopaminergic neuron cell death. Although we detected rotenone induced mitochondrial ultrastructu...
Source: Neurochemistry International - Category: Neuroscience Source Type: research