Neuronal degeneration, mitochondrial dysfunction, and disturbance of movements induced by rotenone in the ascidian Styela plicata.

Parkinson's disease (PD), a movement disorder caused by dopaminergic degeneration in the midbrain, has been induced in various organisms after injection of different neurotoxins, such as rotenone (ROT), which affect mitochondrial complex I. Due to the conserved characteristics of ascidians, these animals constitute an interesting model for comparative and genetic studies of neurodegenerative diseases. In this study, we investigated the effects of ROT on the ascidian nervous system, evaluating apoptosis, catecholaminergic enzymes, behavioral deficits, and mitochondrial dysfunction. The study revealed morphological disorganization, inducing vacuolation in the ascidian brain. Neuronal death was confirmed by elevated transcriptional levels of caspase-3 and intense caspase-3 staining by immunofluorescence. In addition, there was reduced staining for dopa-decarboxylase (DDC), which is involved in dopamine biosynthesis. Furthermore, the mitochondria exhibited dysfunction in their membrane potential, followed by a decrease in the hydrolytic activity of ATP synthase and high transcriptional levels of ubiquitin. Finally, after administration of the drug l-3,4-dihydroxyphenylalanine (L-DOPA), recovery of motor movements was observed, as revealed by behavioral tests. Overall, the current research provides new data on the effects of rotenone on the ascidian brain, inducing neuronal death, mitochondrial dysfunction, and siphon movement disorders in the ascidian Styela plicata.