ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006
Cannabinoid receptor type 1 located on presynaptic terminals of principal neurons in the forebrain controls glutamatergic synaptic transmission.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 103 papers.
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Who cites it
103 citing papers in PubMed, 219 citations in OpenAlex.
- Neuromodulators of orbitofrontal cortex function: A review of endocannabinoid, neurotrophin, and cell adhesion systems.Neurobiology of disease · 2026Review
- Genetic Pathways Point to the Biology Underlying the Association Between Cannabis Use Disorder and Psychosis.Biological psychiatry global open science · 2026Article
- Environmental enrichment reverses ELS-induced visceral pain and depression through a prefrontal-limbic circuit involving CB1Rs.Communications biology · 2026Article
- Interactions Between Plant-Derived Psychoactive Substances andMolecules (Basel, Switzerland) · 2026Review
- Exercise-induced anandamide-CB1R signaling and prefrontal-amygdala stress circuits in adolescent depression: a critical hypothesis-driven narrative review.Frontiers in psychiatry · 2026Review
- Genetic Tools in Rodents to Study Cannabinoid Functions.Current topics in behavioral neurosciences · 2026Review
- Review
- Behavioral Decoding Reveals Cortical Endocannabinoid Potentiation during ΔbioRxiv : the preprint server for biology · 2025Article
- The primary somatosensory sensory cortex-basolateral amygdala pathway contributes to comorbid depression in spared nerve injury-induced neuropathic pain.Scientific reports · 2025Article
- Genetic crosstalk of autism spectrum disorders and epilepsy: an insight into the presynapse.Frontiers in neurology · 2025Article
- Cannabinoids: Role in Neurological Diseases and Psychiatric Disorders.International journal of molecular sciences · 2024Review
- Extracellular glutamate is not modulated by cannabinoid receptor activity.Scientific reports · 2024Article
- Effects of Cannabis on Glutamatergic Neurotransmission: The Interplay between Cannabinoids and Glutamate.Cells · 2024Review
- Effects of Cannabinoids on Intestinal Motility, Barrier Permeability, and Therapeutic Potential in Gastrointestinal Diseases.International journal of molecular sciences · 2024Review
- Conditioning and pseudoconditioning differently change intrinsic excitability of inhibitory interneurons in the neocortex.Cerebral cortex (New York, N.Y. : 1991) · 2024Article
- Synaptotagmin 7 Sculpts Short-Term Plasticity at a High Probability Synapse.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Article
- Control of a hippocampal recurrent excitatory circuit by cannabinoid receptor-interacting protein Gap43.Nature communications · 2023Article
- Differential Regulation of Prelimbic and Thalamic Transmission to the Basolateral Amygdala by Acetylcholine Receptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Cannabinoid receptor 2 evolutionary gene loss makes parrots more susceptible to neuroinflammation.Proceedings. Biological sciences · 2022Article
43 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is widely accepted that cannabinoids regulate GABA release by activation of cannabinoid receptor type 1 (CB1). Results obtained from a variety of brain regions consistently indicate that cannabinoid agonists can also reduce glutamatergic synaptic transmission. However, there are still conflicting data concerning the role of CB1 in cannabinoid-induced inhibition of glutamatergic transmission in cortical areas. Here, we provide direct evidence that activation of CB1 on terminals of principal neurons controls excitatory synaptic responses in the forebrain. In slices of the basolateral amygdala, the CA1 region of the hippocampus, and the primary somatosensory cortex of wild-type mice, application of the CB1 agonist (R)-(+)-[2,3-dihydro-5-methyl-3-(4-morpholinylmethyl)pyrrolo[1,2,3-de]-1,4-benzoxazin-6-yl]-1-naphthalenylmethanone (WIN55,212-2; WIN) (5 mum) reduced evoked excitatory postsynaptic responses. In contrast, in slices obtained from conditional mouse mutants lacking CB1 in all principal forebrain neurons but not in GABAergic interneurons (CB1(f/f;CaMKIIalphaCre)), WIN no longer affected glutamatergic synaptic transmission in any of the brain regions tested. Compatible with a presynaptic mechanism, WIN did not change the sensitivity to focally uncaged l-glutamate. WIN reduced glutamatergic responses in slices obtained from mice lacking CB1 exclusively in GABAergic neurons (CB1(f/f;Dlx5/6-Cre)), thus excluding the involvement of CB1 expressed on GABAergic neurons in this effect of the drug. The present data strongly indicate that excitatory synaptic transmission in forebrain areas is directly modulated by CB1 expressed on presynaptic axon terminals originating from glutamatergic neurons.
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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.