Very excited to share our (@Landgraf10006, @cwbeetle, @CamZoology) @biorxivpreprint investigating reactive oxygen species as novel signals for activity-dependent structural #plasticity in the #Drosophila brain! It’s my first lead-author work! biorxiv.org/content/10.110… 
Following increased neuronal activity, reactive oxygen species (ROS) mediate homeostatic reductions in dendritic arbor size and branching complexity. Here, we implicate the NADPH oxidase Dual Oxidase (Duox) as the source of this ROS.
As Duox generates ROS extracellularly, we wondered if these ROS might need to re-enter the neuron for plasticity to occur. We hypothesized that aquaporin channel proteins might facilitate transmembrane ROS transport and found a requirement for 2 of 3 aquaporins tested.
Excitingly, this is amongst the first work to investigate aquaporins in the context of neuronal plasticity and one of the first characterizations of insect aquaporins outside of their role in fluid homeostasis.
Some of you eagle-eyed folk may have noticed that aquaporin knockdowns without dTrpA1 overactivation cause a curious dendritic overgrowth phenotype. This led us to wonder if extracellular ROS act as negative regulators of growth at basal levels of neuronal activity
Such a model predicts that local quenching of extracellular ROS should have a comparable effect of dendritic growth, which indeed we do find via cell-specific expression of a potent secreted form of the ROS scavenger: catalase.
Overall our findings suggest that neuronal activity leads to activation of Duox, which in turn generates ROS into the extracellular space surrounding the neuron. Aquaporins then channel these ROS into the cytoplasm where they trigger pathways to limit dendritic growth.
Thanks again to @Landgraf10006 @cwbeetle @CamZoology and fellow scientists in arms @Eva_Higg and Matt Oswald (twitterless?!) for all their hard-work and support! Twitter thread over and out!
p.s. your daily dose of sci-comm is partly sponsored by my excellent PR manager @as_bates🤩
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