Docosahexaenoic acid protection in a rotenone induced Parkinson's model: Prevention of tubulin and synaptophysin loss, but no association with mitochondrial function
| Autor: | Tarsila Elizabeth Juárez-Zepeda, Leticia Granados-Rojas, Sandra Orozco-Suárez, Norma Serrano-García, Marisol Orozco-Ibarra, Francisca Fernández-Valverde, José Pedraza-Chaverri, Anabel Jiménez-Anguiano, Erika Rubí Luis-García |
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| Rok vydání: | 2018 |
| Předmět: |
Male
0301 basic medicine Parkinson's disease Docosahexaenoic Acids Synaptophysin Pharmacology Neuroprotection 03 medical and health sciences Cellular and Molecular Neuroscience chemistry.chemical_compound 0302 clinical medicine Parkinsonian Disorders Tubulin Rotenone medicine Animals Rats Wistar biology Tyrosine hydroxylase Uncoupling Agents Parkinsonism Dopaminergic Cell Biology medicine.disease Mitochondria Rats Neuroprotective Agents 030104 developmental biology chemistry Docosahexaenoic acid biology.protein 030217 neurology & neurosurgery |
| Zdroj: | Neurochemistry International. 121:26-37 |
| ISSN: | 0197-0186 |
| DOI: | 10.1016/j.neuint.2018.10.015 |
| Popis: | Rotenone, 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 seven days and then administered rotenone for eight 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 ultrastructure alterations, these were not associated with mitochondrial dysfunction. Rotenone had no effect on mitochondrial complex I, respiratory control ratio, mitochondrial transmembrane potential or ATP production activity. DHA also prevented a rotenone-induced decrease in tubulin and synaptophysin expression. Our results support the neuroprotective effect of DHA on rotenone-induced parkinsonism, and a possible effect on early stage Parkinson's disease. This protective effect is not associated with mitochondrial function improvement, but rather with preventing loss of tubulin and synaptophysin, proteins relevant to synaptic transmission. |
| Databáze: | OpenAIRE |
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