ArticleFrontiers in molecular neuroscience2017
Fyn Signaling Is Compartmentalized to Dopamine D1 Receptor Expressing Neurons in the Dorsal Medial Striatum.
Article in Frontiers in molecular neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Fyn kinase: a key mechanistic regulator and therapeutic target in tauopathy and neurodegenerative diseases.Translational neurodegeneration · 2026Review
- Review
- Cell type-specific gene regulatory atlas prioritizes drug targets and repurposable medicines in Alzheimer's disease.Genome research · 2026Article
- The roles of RACK1 in the pathogenesis of Alzheimer's disease.Journal of biomedical research · 2024Article
- cAMP-Fyn signaling in the dorsomedial striatum direct pathway drives excessive alcohol use.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021Article
- The Fyn kinase inhibitor, AZD0530, suppresses mouse alcohol self-administration and seeking.Addiction biology · 2019Article
- Molecular tools to elucidate factors regulating alcohol use.Alcohol (Fayetteville, N.Y.) · 2019Review
- Amphetamine activates non-receptor tyrosine kinase Fyn and stimulates ERK phosphorylation in the rat striatum in vivo.European journal of pharmacology · 2019Article
- Targeting the intracellular signaling "STOP" and "GO" pathways for the treatment of alcohol use disorders.Psychopharmacology · 2018Review
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Authors and funding
5 authors.
Funding
Abstract
The tyrosine kinase Fyn plays an important role in synaptic plasticity, learning, and memory. Here we report that Fyn is activated in response to 15 min D1 receptor (D1R) but not D2 receptor (D2R) stimulation specifically in the dorsomedial striatum (DMS) of mice but not in the other substriatal regions, the dorsolateral striatum (DLS), and the nucleus accumbens (NAc). Once activated Fyn phosphorylates its substrate GluN2B, and we show that GluN2B is phosphorylated only in the DMS but not in the other striatal regions. Striatal neurons are divided into D1R expressing medium spiny neurons (MSNs) and D2R expressing MSNs. Thus, to explore the cell-type specificity of this signaling pathway in the DMS, we developed a Cre-dependent Flip Excision (FLEX) approach to knockdown Fyn in D1R MSNs or D2R MSNs, and proved that the D1R-dependent Fyn activation is localized to DMS D1R MSNs. Importantly, we provide evidence to suggest that the differential association of Fyn and GluN2B with the scaffolding RACK1 is due to the differential localization of Fyn in lipid rafts.Our data further suggest that the differential cholesterol content in the three striatal regions may determine the region specificity of this signaling pathway. Together, our data show that the D1R-dependent Fyn/GluN2B pathway is selectively activated in D1R expressing MSNs in the DMS, and that the brain region specificity of pathway depends on the molecular and cellular compartmentalization of Fyn and GluN2B.
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