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SUSCEPTIBILITY OF DOPAMINERGIC NERVE TERMINALS TO MITOCHONDRIAL DYSFUNCTION
Maya Faourand 2 co-authors
Paris Brain Institute
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS06-09PM-618
Presentation
Date TBA
Board: PS06-09PM-618
Event Information
Poster Board
PS06-09PM-618
Poster
View posterAbstract
Dopaminergic (DA) neurons of the substantia nigra pars compacta (SNc) exhibit a pronounced vulnerability to mitochondrial dysfunction, yet the causal mechanisms underlying this susceptibility remain poorly understood. In this project, we investigate how impaired mitochondrial metabolism contributes to dopaminergic dysfunction by selectively disrupting mitochondrial Complex I in SNc DA neurons. This is achieved through targeted knockdown of the Ndufs2 subunit, a critical component of Complex I, an approach motivated by recent evidence linking Complex I impairment to progressive parkinsonian phenotypes. Using DAT-Cre mice, we assess the functional consequences of mitochondrial dysfunction on dopaminergic neurotransmission by monitoring dopamine release dynamics in the dorsal striatum in vivo. Fiber photometry recordings of the genetically encoded dopamine sensor GRAB-DA are performed during behavioral tasks to quantify activity-dependent dopamine signaling under physiological conditions. These experiments enable us to establish a direct link between mitochondrial impairment and altered dopaminergic output. Overall, this work aims to elucidate the cellular mechanisms underlying the intrinsic vulnerability of dopaminergic neurons in Parkinson’s disease and to lay the groundwork for a high-impact publication in the field of neurodegeneration.
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