ArticleProceedings of the National Academy of Sciences of the United States of America2013
Nerve growth factor scales endocannabinoid signaling by regulating monoacylglycerol lipase turnover in developing cholinergic neurons.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 47 citations in OpenAlex.
- Review
- Article
- Physiological Rules of Endocannabinoid Action During Fetal and Neonatal Brain Development.Cannabis and cannabinoid research · 2021Article
- Genetic Manipulation of sn-1-Diacylglycerol Lipase and CBCannabis and cannabinoid research · 2021Article
- Interference with the Cannabinoid Receptor CB1R Results in Miswiring of GnRH3 and AgRP1 Axons in Zebrafish Embryos.International journal of molecular sciences · 2019Article
- 2-Linoleoylglycerol Is a Partial Agonist of the Human Cannabinoid Type 1 Receptor that Can Suppress 2-Arachidonolyglycerol and Anandamide Activity.Cannabis and cannabinoid research · 2019Article
- A BRCA1-Dependent DNA Damage Response in the Regenerating Adult Peripheral Nerve Milieu.Molecular neurobiology · 2018Article
- Brca1 Is Upregulated by 5-Aza-CdR and Promotes DNA Repair and Cell Survival, and Inhibits Neurite Outgrowth in Rat Retinal Neurons.International journal of molecular sciences · 2018Article
- Article
- The role of cannabinoids in adult neurogenesis.British journal of pharmacology · 2015Review
- Postnatal ethanol exposure alters levels of 2-arachidonylglycerol-metabolizing enzymes and pharmacological inhibition of monoacylglycerol lipase does not cause neurodegeneration in neonatal mice.Journal of neurochemistry · 2015Article
- BRCA1 and p53 tumor suppressor molecules in Alzheimer's disease.International journal of molecular sciences · 2015Review
- The Endocannabinoid Signaling System in the CNS: A Primer.International review of neurobiology · 2015Review
- Therapeutic potential of inhibitors of endocannabinoid degradation for the treatment of stress-related hyperalgesia in an animal model of chronic pain.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2015Article
- Programming of neural cells by (endo)cannabinoids: from physiological rules to emerging therapies.Nature reviews. Neuroscience · 2014Review
- GABAergic terminals are a source of galanin to modulate cholinergic neuron development in the neonatal forebrain.Cerebral cortex (New York, N.Y. : 1991) · 2014Article
- Neuronal substrates and functional consequences of prenatal cannabis exposure.European child & adolescent psychiatry · 2014Review
- Article
- Miswiring the brain: Δ9-tetrahydrocannabinol disrupts cortical development by inducing an SCG10/stathmin-2 degradation pathway.The EMBO journal · 2014Article
- CB1 cannabinoid receptors couple to focal adhesion kinase to control insulin release.The Journal of biological chemistry · 2013Article
Corrections and comments
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Authors and funding
11 authors at 7 institutions in 5 countries.
Funding
Abstract
Endocannabinoid, particularly 2-arachidonoyl glycerol (2-AG), signaling has recently emerged as a molecular determinant of neuronal migration and synapse formation during cortical development. However, the cell type specificity and molecular regulation of spatially and temporally confined morphogenic 2-AG signals remain unexplored. Here, we demonstrate that genetic and pharmacological manipulation of CB(1) cannabinoid receptors permanently alters cholinergic projection neuron identity and hippocampal innervation. We show that nerve growth factor (NGF), implicated in the morphogenesis and survival of cholinergic projection neurons, dose-dependently and coordinately regulates the molecular machinery for 2-AG signaling via tropomyosine kinase A receptors in vitro. In doing so, NGF limits the sorting of monoacylglycerol lipase (MGL), rate limiting 2-AG bioavailability, to proximal neurites, allowing cell-autonomous 2-AG signaling at CB(1) cannabinoid receptors to persist at atypical locations to induce superfluous neurite extension. We find that NGF controls MGL degradation in vitro and in vivo and identify the E3 ubiquitin ligase activity of breast cancer type 1 susceptibility protein (BRCA1) as a candidate facilitating MGL's elimination from motile neurite segments, including growth cones. BRCA1 inactivation by cisplatin or genetically can rescue and reposition MGL, arresting NGF-induced growth responses. These data indicate that NGF can orchestrate endocannabinoid signaling to promote cholinergic differentiation and implicate BRCA1 in determining neuronal morphology.
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