Octopamine (analogue of noradrenaline in mammals) is a neurotransmitter that regulates many physiological processes in the fruit fly or Drosophila. It triggers intracellular Ca2+ and cAMP signaling by binding to octopamine/tyramine G protein-coupled receptors. The effect of octopamine on intracellular signaling and metabolism in neuroglial cells in the adult Drosophila brain has not yet been investigated. Using confocal microscopy and genetically encoded nanosensors, we monitored changes in intracellular Ca2+, cAMP, D-glucose and L-lactate concentrations in neuroglial cells and in neurons in the brains of young and aged Drosophila. We demonstrated that brain stimulation with octopamine triggers an increase in intracellular Ca2+ concentration in astrocyte-like glia (ALG) in the brain of young Drosophila, most likely via Octα1R and/or Tyr1R. Ca2+ signaling upon octopamine stimulation is impaired in ALG in the brain of aged Drosophila. In the brain of young Drosophila, octopamine triggers an increase in intracellular cAMP concentration in neurons, most likely via OctβR octopamine receptors, while we did not detect changes in intracellular cAMP concentration in ALG. Neuroglial cells and neurons in the brain of young Drosophila efficiently take up extracellular D-glucose and L-lactate, whereas in the brain of aged Drosophila, D-glucose uptake by neurons is reduced, which may contribute to the hypometabolism. Octopamine induce an increase in intracellular D-glucose concentration in ALG in brains of young Drosophila, while no increase was observed in brains of aged Drosophila. In contrast, octopamine does not trigger an increase in intracellular L-lactate concentration, suggesting that octopamine does not stimulate aerobic glycolysis in the ALG. Our aim was also to investigate how stress factors characteristic of CNS disease and aging affect lipid metabolism in the Drosophila brain. Exposure of Drosophila to hypoxia and metabolic stress leads to accumulation of lipid droplets (LD) in neuroglial cells, suggesting an involvement of neuroglial cells in LD metabolism under stress conditions.
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