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The HSPG Glypican Regulates Experience-Dependent Synaptic and Behavioral Plasticity by Modulating the Non-Canonical
Keisuke Kamimura1, Aiko Odajima1, Yuko Ikegawa1
1Neural Network Project, Department of Brain Development and Neural Regeneration, Tokyo Metropolitan Institute of Medical Science, Setagaya, Tokyo 156-8506, Japan.
Cell Reports
|September 19, 2019
Summary
Food deprivation increases Drosophila larval speed and synapse growth. Octopamine signaling reduces glypican (Dlp) expression, enhancing neural plasticity and locomotion by modulating the BMP pathway.
Area of Science:
- Neuroscience
- Developmental Biology
- Molecular Biology
Background:
- Food deprivation triggers increased locomotor speed and synaptic growth in Drosophila larvae.
- Octopamine is implicated in this starvation response, but its precise molecular mechanisms are unknown.
Purpose of the Study:
- To elucidate the role of glypican (Dlp) in mediating starvation-induced neural and behavioral plasticity in Drosophila.
- To investigate the molecular pathway through which octopaminergic signaling influences synaptic formation and locomotion.
Main Methods:
- Genetic manipulation of glypican (Dlp) expression in Drosophila.
- Analysis of synaptic bouton numbers at neuromuscular junctions (NMJs).
- Assessment of postsynaptic GluRIIA expression and larval locomotor behavior.
Main Results:
- Glypican (Dlp) negatively regulates synaptic bouton formation, GluRIIA expression, and locomotor speed.
- Starvation-induced octopaminergic signaling decreases Dlp expression.
- Reduced Dlp enhances non-canonical BMP signaling, leading to increased GluRIIA, bouton number, and locomotion.
Conclusions:
- Octopamine controls starvation-induced neural plasticity by regulating Dlp expression.
- Dlp acts as a suppressor of the non-canonical BMP pathway.
- Proteoglycans like Dlp play a significant role in modulating behavioral and synaptic plasticity during starvation.
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