Open access
Date
2021-12-14Type
- Journal Article
Abstract
Presynaptic homeostatic plasticity (PHP) stabilizes synaptic transmission by counteracting impaired neurotransmitter receptor function through neurotransmitter release potentiation. PHP is thought to be triggered by impaired receptor function and to involve a stereotypic signaling pathway. However, here we demonstrate that different receptor perturbations that similarly reduce synaptic transmission result in different responses at the Drosophila neuromuscular junction. While receptor inhibition by the glutamate receptor (GluR) antagonist g-D-glutamylglycine (gDGG) is not compensated by PHP, the GluR inhibitors Philanthotoxin-433 (PhTx) and Gyki-53655 (Gyki) induce compensatory PHP. Intriguingly, PHP triggered by PhTx and Gyki involve separable signaling pathways, including inhibition of distinct GluR subtypes, differential modulation of the active zone scaffold Bruchpilot, and short-term plasticity. Moreover, while PHP upon Gyki treatment does not require genes promoting PhTx-induced PHP, it involves presynaptic protein kinase D. Thus, synapses not only respond differentially to similar activity impairments, but achieve homeostatic compensation via distinct mechanisms, highlighting the diversity of homeostatic signaling. Show more
Permanent link
https://doi.org/10.3929/ethz-b-000523728Publication status
publishedExternal links
Journal / series
Cell ReportsVolume
Pages / Article No.
Publisher
Cell PressSubject
synaptic transmission; neurotransmitter release; glutamate receptors; homeostatic plasticity; Protein Kinase D; Drosophila neuromuscular junctionMore
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