ArticleNature neuroscience2026
Distinct endocannabinoids specifically signal to astrocytes or neurons in the adult mouse hippocampus.
Article in Nature neuroscience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed.
- Article
- Dissociable control of depression and visceral pain by the pICNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- Inhibition of endocannabinoid degradation in astrocytes reprograms glial reactivity and prevents seizure sequelae.Journal of neuroinflammation · 2026Article
- Towards Mechanism-Informed Treatments for Mental Health.Journal of neurochemistry · 2026Review
- Multiple Roles of Cannabinoids in the Olfactory System.Brain sciences · 2026Review
- The how and why for multiple forms of hippocampal LTP.Frontiers in synaptic neuroscience · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors.
Funding
Abstract
The endocannabinoid (eCB) system is involved in many processes in brain function. eCBs depress synaptic transmission by directly activating presynaptic CB1 receptors (CB1Rs), and they indirectly potentiate adjacent synapses by activating astrocytic CB1Rs. In contrast to other neurotransmitter systems, the brain eCB system involves two endogenous ligands, 2-arachidonoylglycerol (2-AG) and anandamide (AEA), and the receptor CB1R. The meaning of this particularity remains unknown. Here we show that 2-AG selectively signals to neurons, eliciting the depression, which is mediated exclusively by neuronal mechanisms. By contrast, AEA signals to astrocytes, inducing lateral synaptic potentiation. Moreover, AEA, but not 2-AG, and astrocyte-mediated signaling are required for hippocampal spike-timing-dependent long-term potentiation. Hence, while 2-AG selectively signals to neurons, AEA specifically signals to astrocytes, evoking contrasting regulatory phenomena of synaptic transmission and plasticity. These results reveal distinct cell-type-specific signaling pathways that involve unique eCBs selectively signaling to either neurons or astrocytes.
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What Socratic holds
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 Socratic graph.