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FATTY ACID OXIDATION REGULATES MITOCHONDRIAL DYNAMICS AND CALCIUM SIGNALS IN ASTROCYTES
Francina Bagur-Llufriuand 4 co-authors
Universitat Autònoma de Barcelona
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS04-08PM-226
Presentation
Date TBA
Board: PS04-08PM-226
Event Information
Poster Board
PS04-08PM-226
Poster
View posterAbstract
Metabolic changes are vitally important for brain plasticity and cognitive functions. Fatty acid oxidative metabolism (FAO) in astrocytes is emerging as a key brain energy pathway which could be dysregulated in neurodegeneration. However, the implications of using different energy substrates for astrocyte and neuronal physiology remain largely unexplored. Here we aimed to elucidate how FAO shapes astrocytic physiology. We show that cultured astrocytes oxidise 3H-palmitate in the presence of glucose, albeit there is a more active FAO in the absence of glucose. Accordingly, inhibition of FAO with 4 μM etomoxir for 2 hours induces accumulation of lipid droplets labelled with BODIPY. On the other hand, real time fluorescent microscopy studies with Mitotracker showed that 4 μM etomoxir and 100μM glutamate, which inhibits FAO by 70%, also promote mitochondrial fission as they increase number of mitochondria with smaller area and perimeter. Moreover, the presence of 4 μM etomoxir decreases purinergic-induced intracellular calcium signals. Importantly, in mixed astrocytic-neuronal cultures, astrocytic FAO inhibition modules neuronal calcium responses, suggesting that astrocytic FAO might modulate astrocyte-neuronal communication. In conclusion, astrocytes oxidase fatty acids at physiological conditions and this FAO is necessary to fulfil astrocytic functions.
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