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Behavioral Assessments of Spontaneous Locomotion in a Murine MPTP-induced Parkinson's Disease Model
Published on: January 7, 2019
Mortalin inhibition in experimental Parkinson's disease
Davide Chiasserini1, Alessandro Tozzi, Antonio de Iure
1Clinica Neurologica, Università degli studi di Perugia, Ospedale S. Maria della Misericordia, Perugia, Italy.
Summary
Mortalin, a heat shock protein, is downregulated in Parkinson's disease models. Inhibiting mortalin with MKT-077 affects neuronal activity, especially in conditions mimicking Parkinson's disease, suggesting a role in mitochondrial function.
Area of Science:
- Neuroscience
- Molecular Biology
- Biochemistry
Background:
- Mortalin, a heat shock protein, is implicated in the pathogenesis of Parkinson's disease.
- Understanding mortalin's role in Parkinson's disease requires investigating its expression and function in relevant models.
Purpose of the Study:
- To analyze striatal protein expression, specifically mortalin, in a rat model of Parkinson's disease.
- To investigate the involvement of mortalin in Parkinson's disease pathogenesis using electrophysiology and pharmacological inhibition.
Main Methods:
- Proteomic analysis of striatal protein expression in the 6-hydroxydopamine (6-OHDA) rat model of Parkinson's disease.
- Electrophysiological recordings (field potential) from corticostriatal brain slices.
- Pharmacological inhibition of mortalin using MKT-077 in physiological and parkinsonian states, with and without rotenone.
Main Results:
- Proteomic analysis revealed downregulation of mortalin in the striata of 6-OHDA-treated rats.
- MKT-077 reduced corticostriatal field potential amplitude in physiological conditions, causing membrane depolarization.
- MKT-077 induced significant changes in parkinsonian slices and slices treated with rotenone (mitochondrial inhibitor) at concentrations not affecting physiological conditions.
Conclusions:
- Mortalin expression is reduced in a rat model of Parkinson's disease.
- Mortalin inhibition impacts neuronal excitability, particularly under conditions mimicking Parkinson's disease and mitochondrial dysfunction.
- Findings suggest a critical link between mortalin function and mitochondrial activity in physiological and Parkinson's disease-like states.
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