ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008
Roles of calcium-stimulated adenylyl cyclase and calmodulin-dependent protein kinase IV in the regulation of FMRP by group I metabotropic glutamate receptors.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 36 citations in OpenAlex.
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- Analgesic effects of adenylyl cyclase inhibitor NB001 on bone cancer pain in a mouse model.Molecular pain · 2016Article
- GABAB receptor upregulates fragile X mental retardation protein expression in neurons.Scientific reports · 2015Article
- Activity-dependent FMRP requirements in development of the neural circuitry of learning and memory.Development (Cambridge, England) · 2015Article
- Targeted pharmacological treatment of autism spectrum disorders: fragile X and Rett syndromes.Frontiers in cellular neuroscience · 2015Review
- Fragile X mental retardation protein: from autism to neurodegenerative disease.Frontiers in cellular neuroscience · 2015Article
- GluA1 phosphorylation contributes to postsynaptic amplification of neuropathic pain in the insular cortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Postsynaptic activity reverses the sign of the acetylcholine-induced long-term plasticity of GABAA inhibition.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Common variants in genes of the postsynaptic FMRP signalling pathway are risk factors for autism spectrum disorders.Human genetics · 2014Article
- Lipid rafts: a signaling platform linking cholesterol metabolism to synaptic deficits in autism spectrum disorders.Frontiers in behavioral neuroscience · 2014Article
- Impaired activity-dependent neural circuit assembly and refinement in autism spectrum disorder genetic models.Frontiers in cellular neuroscience · 2014Review
- Fear extinction induces mGluR5-mediated synaptic and intrinsic plasticity in infralimbic neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Roles of CREB in the regulation of FMRP by group I metabotropic glutamate receptors in cingulate cortex.Molecular brain · 2012Article
- Therapeutic strategies in fragile X syndrome: dysregulated mGluR signaling and beyond.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2012Review
- Group I metabotropic glutamate receptor-mediated gene transcription and implications for synaptic plasticity and diseases.Frontiers in pharmacology · 2012Article
- Fragile X syndrome and targeted treatment trials.Results and problems in cell differentiation · 2012Review
- Targeted treatments for fragile X syndrome.Journal of neurodevelopmental disorders · 2011Article
- The fragile X mental retardation protein developmentally regulates the strength and fidelity of calcium signaling in Drosophila mushroom body neurons.Neurobiology of disease · 2011Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The fragile X syndrome is caused by the lack of fragile X mental retardation protein (FMRP) attributable to silencing of the FMR1 gene. The metabotropic glutamate receptors (mGluRs) in the CNS contribute to different brain functions, including learning/memory, mental disorders, drug addiction, and persistent pain. Most of the previous studies have been focused on downstream targets of FMRP in hippocampal neurons, and fewer studies have been reported for the second-messenger signaling pathways between group I mGluRs and FMRP. Furthermore, no molecular study has been performed in the anterior cingulate cortex (ACC), a key region involved in high brain cognitive and executive functions. In this study, we demonstrate that activation of group I mGluR upregulated FMRP in ACC neurons of adult mice through the Ca(2+)-dependent signaling pathways. Using genetic approaches, we found that Ca(2+)/calmodulin-stimulated adenylyl cyclase 1 (AC1) and calcium/calmodulin-dependent kinase IV (CaMKIV) contribute to the upregulation of FMRP induced by stimulating group I mGluRs. The upregulation of FMRP occurs at the transcriptional level. The cAMP-dependent protein kinase is activated by stimulating group I mGluRs through AC1 in ACC neurons. Both AC1 and CaMKIV contribute to the regulation of FMRP by group I mGluRs probably through cAMP response element-binding protein activation. Our study has provided the first evidence for a molecular link between group I mGluRs and FMRP in ACC neurons and may help us to understand the pathogenesis of fragile X syndrome.
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