ArticleThe Journal of clinical investigation2020
An endocannabinoid-regulated basolateral amygdala-nucleus accumbens circuit modulates sociability.
Article in The Journal of clinical investigation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
78 citing papers in PubMed, 1 synthesis or guideline pooled it, 119 citations in OpenAlex.
- Alterations of the endocannabinoid system in autism spectrum disorder: a systematic review and meta-analysis.European archives of psychiatry and clinical neuroscience · 2025Pooled it
- Children and adolescents with ASD treated with CBD-rich cannabis exhibit significant improvements particularly in social symptoms: an open label study.Translational psychiatry · 2022Trial
- Emotional Responses (Intensity/Valence) Fulfill RDoC Criteria but Remain Excluded From Diagnostic Classifications of Mood Disorders.Bipolar disorders · 2026Review
- Cell-type-specific disruption of nucleus accumbens social representations in a mouse model of autism.Neuron · 2026Article
- Proximity in mice induced by an auditory-conditioned stimulus.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- Article
- Social Novelty Recruits a Dysfunctional Nucleus Accumbens Ensemble That Drives Social Avoidance in abioRxiv : the preprint server for biology · 2026Article
- FOXG1 Hierarchically Shapes Synaptic Functions in Striatal iSPNs and Contributes to ASD Etiology.Neuroscience bulletin · 2026Article
- CB1 receptor signaling at the cingulate-striatal circuit is anxiogenic.Nature communications · 2026Article
- Divergent BLA engram circuits orchestrate social preference dynamics in bystander male mice with self-experienced stress.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Affiliation in mice induced by an auditory-conditioned stimulus.bioRxiv : the preprint server for biology · 2026Article
- Deficiency of Shank3 in the nucleus accumbens reveals a loss of social-specific motivation.Communications biology · 2025Article
- A network of basolateral amygdala projection neurons contributes to stress-induced activation of the hypothalamic-pituitary-adrenal axis.Science advances · 2025Article
- Gain of Alternative Allele Expression of LINC02449 at rs149707223 in Schizophrenia and Bipolar Disorder: Inducing Synaptic Transmission and Behavioral Deficits in Mice.Nature communications · 2025Article
- Risk reshapes amygdala representation of choice.bioRxiv : the preprint server for biology · 2025Article
- Organization of Brainwide Inputs to Discrete Lateral Septum Projection Populations.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- IRF8 deficiency causes anxiety-like behavior in a sex-dependent manner.bioRxiv : the preprint server for biology · 2025Article
- Potentiation of Nigra-Striatal Dopaminergic Projection Underpins Core Autism-Like Behaviors in Valproate-Exposed Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Ppp2r1a haploinsufficiency increases excitatory synaptic transmission and decreases spatial learning by impairing endocannabinoid signaling.The Journal of clinical investigation · 2025Article
- A cell-type-specific epigenetic mechanism encodes social investigatory behavior via Lrhcn1 and Hcn1.Science advances · 2025Article
18 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
Deficits in social interaction (SI) are a core symptom of autism spectrum disorders (ASDs); however, treatments for social deficits are notably lacking. Elucidating brain circuits and neuromodulatory signaling systems that regulate sociability could facilitate a deeper understanding of ASD pathophysiology and reveal novel treatments for ASDs. Here we found that in vivo optogenetic activation of the basolateral amygdala-nucleus accumbens (BLA-NAc) glutamatergic circuit reduced SI and increased social avoidance in mice. Furthermore, we found that 2-arachidonoylglycerol (2-AG) endocannabinoid signaling reduced BLA-NAc glutamatergic activity and that pharmacological 2-AG augmentation via administration of JZL184, a monoacylglycerol lipase inhibitor, blocked SI deficits associated with in vivo BLA-NAc stimulation. Additionally, optogenetic inhibition of the BLA-NAc circuit markedly increased SI in the Shank3B-/- mouse, an ASD model with substantial SI impairment, without affecting SI in WT mice. Finally, we demonstrated that JZL184 delivered systemically or directly to the NAc also normalized SI deficits in Shank3B-/- mice, while ex vivo JZL184 application corrected aberrant NAc excitatory and inhibitory neurotransmission and reduced BLA-NAc-elicited feed-forward inhibition of NAc neurons in Shank3B-/- mice. These data reveal circuit-level and neuromodulatory mechanisms regulating social function relevant to ASDs and suggest 2-AG augmentation could reduce social deficits via modulation of excitatory and inhibitory neurotransmission in the NAc.
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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.