ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
Cell death triggers olfactory circuit plasticity via glial signaling in Drosophila.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
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- A GAL80 Collection To Inhibit GAL4 Transgenes inG3 (Bethesda, Md.) · 2018Article
- Role of Glial Immunity in Lifespan Determination: AFrontiers in immunology · 2018Review
- Fibroblast growth factor signaling instructs ensheathing glia wrapping ofProceedings of the National Academy of Sciences of the United States of America · 2017Article
- A Population of Projection Neurons that Inhibits the Lateral Horn but Excites the Antennal Lobe through Chemical Synapses inFrontiers in neural circuits · 2017Article
- Glia in Drosophila behavior.Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology · 2015Review
- Drosophila Central Nervous System Glia.Cold Spring Harbor perspectives in biology · 2015Review
- Early olfactory processing in Drosophila: mechanisms and principles.Annual review of neuroscience · 2013Review
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- Gap junction-mediated electrical transmission: regulatory mechanisms and plasticity.Biochimica et biophysica acta · 2013Review
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Authors and funding
3 authors at 2 institutions in 3 countries.
Funding
Abstract
The Drosophila antennal lobe is organized into glomerular compartments, where olfactory receptor neurons synapse onto projection neurons. Projection neuron dendrites also receive input from local neurons, which interconnect glomeruli. In this study, we investigated how activity in this circuit changes over time when sensory afferents are chronically removed in vivo. In the normal circuit, excitatory connections between glomeruli are weak. However, after we chronically severed receptor neuron axons projecting to a subset of glomeruli, we found that odor-evoked lateral excitatory input to deafferented projection neurons was potentiated severalfold. This was caused, at least in part, by strengthened electrical coupling from excitatory local neurons onto projection neurons, as well as increased activity in excitatory local neurons. Merely silencing receptor neurons was not sufficient to elicit these changes, implying that severing receptor neuron axons is the relevant signal. When we expressed the neuroprotective gene Wallerian degeneration slow (Wld(S)) in receptor neurons before severing their axons, this blocked the induction of plasticity. Because expressing Wld(S) prevents severed axons from recruiting glia, this result suggests a role for glia. Consistent with this, we found that blocking endocytosis in ensheathing glia blocked the induction of plasticity. In sum, these results reveal a novel injury response whereby severed sensory axons recruit glia, which in turn signal to central neurons to upregulate their activity. By strengthening excitatory interactions between neurons in a deafferented brain region, this mechanism might help boost activity to compensate for lost sensory input.
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