ArticleScientific reports2015
Fine-tuning of synaptic upscaling at excitatory synapses by endocannabinoid signaling is mediated via the CB1 receptor.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 28 citations in OpenAlex.
- Article
- Lipid droplet accumulation in microglia and their potential roles.Lipids in health and disease · 2025Review
- Cannabinoid Modulation of Excitability and Short-Term Neuronal Dynamics in the Dorsal and Ventral Hippocampus.Biology · 2025Article
- Inhibiting degradation of 2-arachidonoylglycerol as a therapeutic strategy for neurodegenerative diseases.Pharmacology & therapeutics · 2023Review
- Inhibition of 2-arachidonoylglycerol degradation enhances glial immunity by single-cell transcriptomic analysis.Journal of neuroinflammation · 2023Article
- Memory destabilization during reconsolidation: a consequence of homeostatic plasticity?Learning & memory (Cold Spring Harbor, N.Y.) · 2021Article
- Inhibition of 2-Arachidonoylglycerol Metabolism Alleviates Neuropathology and Improves Cognitive Function in a Tau Mouse Model of Alzheimer's Disease.Molecular neurobiology · 2021Article
- Alleviation of Neuropathology by Inhibition of Monoacylglycerol Lipase in APP Transgenic Mice Lacking CB2 Receptors.Molecular neurobiology · 2018Article
- Cannabinoid Modulation of the Stressed Hippocampus.Frontiers in molecular neuroscience · 2017Review
- Article
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Authors and funding
3 authors at 1 institution in 1 country.
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Abstract
The endocannabinoid 2-arachidonoylglycerol (2-AG) functions as a retrograde signaling molecule mediating synaptic transmission and plasticity at both inhibitory and excitatory synapses. However, little is known about whether 2-AG signaling is involved in homeostatic regulation of miniature synaptic events at excitatory synapses in response to activity deprivation. Here, we report that chronic blockade of firing by tetrodotoxin (TTX) for two days resulted in increases both in the frequency and amplitude of spontaneous miniature excitatory postsynaptic currents (mEPSCs) in cultured mouse hippocampal neurons. However, treatment with 2-AG alone or JZL184, a potent and selective inhibitor for monoacylglycerol lipase (MAGL) that hydrolyzes 2-AG, induced a CB1 receptor-dependent reduction of the frequency of mEPSCs, but not the amplitude. The TTX-increased frequency was blunted by 2-AG or JZL184 and this effect was eliminated by pharmacological or genetic inhibition of CB1 receptors. In addition, TTX still increased frequency and amplitude of mEPSCs in the presence of CB1 receptor inhibition. Our results suggest that while endocannabinoids are not required for induction of synaptic scaling at excitatory glutamate synapses after chronic activity deprivation, 2-AG signaling may play a role in fine-tuning of synaptic strengths via presynaptically-expressed CB1 receptors.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.