ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2021
Cannabinoid CB1 receptor in dorsal telencephalic glutamatergic neurons drives overconsumption of palatable food and obesity.
Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Brain cannabinoid CB1 receptor signaling modulates reward responses and inhibitory control in humans.Imaging neuroscience (Cambridge, Mass.) · 2026Article
- Genetic Tools in Rodents to Study Cannabinoid Functions.Current topics in behavioral neurosciences · 2026Review
- The Endocannabinoid System in the Development and Treatment of Obesity: Searching for New Ideas.International journal of molecular sciences · 2025Review
- Functional and evolutionary characteristics of human genes encoding cell surface receptors involved in the regulation of appetite.Journal of integrative bioinformatics · 2025Article
- Endocannabinoid System and Metabolism: The Influences of Sex.International journal of molecular sciences · 2024Review
- Spinal afferent neurons: emerging regulators of energy balance and metabolism.Frontiers in molecular neuroscience · 2024Review
- The Role of the Endocannabinoid System in Binge Eating Disorder.International journal of molecular sciences · 2023Review
- Up-regulation of CBFrontiers in neuroanatomy · 2022Article
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Authors and funding
10 authors at 4 institutions in 2 countries.
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No grant is acknowledged in the PubMed record.
Abstract
Palatable food can promote overfeeding beyond homeostatic requirements, thereby constituting a major risk to obesity. Here, the lack of cannabinoid type 1 receptor (CB1) in dorsal telencephalic glutamatergic neurons (Glu-CB1-KO) abrogated the overconsumption of palatable food and the development of obesity. On low-fat diet, no genotype differences were observed. However, under palatable food conditions, Glu-CB1-KO mice showed decreased body weight and food intake. Notably, Glu-CB1-KO mice were protected from alterations in the reward system after high-fat diet feeding. Interestingly, obese wild-type mice showed a superior olfactory detection as compared to mutant mice, suggesting a link between overconsumption of palatable food and olfactory function. Reconstitution of CB1 expression in olfactory cortex in high-fat diet-fed Glu-CB1-KO mice using viral gene delivery partially reversed the lean phenotype concomitantly with improved odor perception. These findings indicate that CB1 in cortical glutamatergic neurons regulates hedonic feeding, whereby a critical role of the olfactory cortex was uncovered as an underlying mechanism.
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