ArticleiScience2024
Chronic modulation of cAMP signaling elicits synaptic scaling irrespective of activity.
Article in iScience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed.
- Dopaminergic tone inhibits spontaneous glutamate release and augments homeostatic synaptic plasticity.Molecular psychiatry · 2026Article
- Regulation of spontaneous neurotransmission and homeostatic synaptic plasticity by synaptotagmin-1 disease variants at the SNARE primary interface.bioRxiv : the preprint server for biology · 2026Article
- Impact of distinct neurotransmitter release modes on neuronal signaling.Molecular psychiatry · 2026Review
- Histone variant H2BE controls activity-dependent gene expression and homeostatic scaling.Cell reports · 2026Article
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Authors and funding
2 authors.
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Abstract
Homeostatic plasticity mechanisms act in a negative feedback manner to stabilize neuronal firing around a set point. Classically, homeostatic synaptic plasticity is elicited via rather drastic manipulation of activity in a neuronal population. Here, we employed a chemogenetic approach to regulate activity via eliciting G protein-coupled receptor (GPCR) signaling in hippocampal neurons to trigger homeostatic synaptic plasticity. We demonstrate that chronic activation of hM4D(Gi) signaling induces mild and transient activity suppression, yet still triggers synaptic upscaling akin to tetrodotoxin (TTX)-induced complete activity suppression. Therefore, this homeostatic regulation was irrespective of Gi-signaling regulation of activity, but it was mimicked or occluded by direct manipulation of cyclic AMP (cAMP) signaling in a manner that intersected with the retinoic acid receptor alpha (RARα) signaling pathway. Our data suggest chemogenetic tools can uniquely be used to probe cell-autonomous mechanisms of synaptic scaling and operate via direct modulation of second messenger signaling bypassing activity regulation.
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