ArticleJournal of neurochemistry2014
Inhibition of striatal-enriched tyrosine phosphatase 61 in the dorsomedial striatum is sufficient to increased ethanol consumption.
Article in Journal of neurochemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 27 citations in OpenAlex.
- Alcohol effects on associative and sensorimotor cortico-thalamo-basal ganglia circuits alter decision making and alcohol intake.Alcohol (Fayetteville, N.Y.) · 2025Review
- The Src-Kinase Fyn is Required for Cocaine-Associated Memory Through Regulation of Tau.Frontiers in pharmacology · 2022Article
- Three Weeks of Binge Alcohol Drinking Generates Increased Alcohol Front-Loading and Robust Compulsive-Like Alcohol Drinking in Male and Female C57BL/6J Mice.Alcoholism, clinical and experimental research · 2021Article
- cAMP-Fyn signaling in the dorsomedial striatum direct pathway drives excessive alcohol use.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021Article
- Saracatinib Fails to Reduce Alcohol-Seeking and Consumption in Mice and Human Participants.Frontiers in psychiatry · 2021Article
- Chromatin accessibility mapping of the striatum identifies tyrosine kinase FYN as a therapeutic target for heroin use disorder.Nature communications · 2020Article
- Neural Mechanisms Underlying the Rewarding and Therapeutic Effects of Ketamine as a Treatment for Alcohol Use Disorder.Frontiers in behavioral neuroscience · 2020Article
- 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
- Increasing Brain-Derived Neurotrophic Factor (BDNF) in medial prefrontal cortex selectively reduces excessive drinking in ethanol dependent mice.Neuropharmacology · 2018Article
- Targeting the intracellular signaling "STOP" and "GO" pathways for the treatment of alcohol use disorders.Psychopharmacology · 2018Review
- mTORC2 in the dorsomedial striatum of mice contributes to alcohol-dependent F-Actin polymerization, structural modifications, and consumption.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2018Article
- Adenylyl Cyclase 1 Is Required for Ethanol-Induced Locomotor Sensitization and Associated Increases in NMDA Receptor Phosphorylation and Function in the Dorsal Medial Striatum.The Journal of pharmacology and experimental therapeutics · 2017Article
- Alcohol-dependent molecular adaptations of the NMDA receptor system.Genes, brain, and behavior · 2017Review
- Molecular mechanisms underlying alcohol-drinking behaviours.Nature reviews. Neuroscience · 2016Review
- Habitual Alcohol Seeking: Neural Bases and Possible Relations to Alcohol Use Disorders.Alcoholism, clinical and experimental research · 2016Review
- Molecular underpinnings of neurodegenerative disorders: striatal-enriched protein tyrosine phosphatase signaling and synaptic plasticity.F1000Research · 2016Review
- Role of Striatal-Enriched Tyrosine Phosphatase in Neuronal Function.Neural plasticity · 2016Review
- Alcohol Elicits Functional and Structural Plasticity Selectively in Dopamine D1 Receptor-Expressing Neurons of the Dorsomedial Striatum.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Striatal-enriched protein tyrosine phosphatase regulates the PTPα/Fyn signaling pathway.Journal of neurochemistry · 2015Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
The STriatal-Enriched protein tyrosine Phosphatase 61 (STEP61 ) inhibits the activity of the tyrosine kinase Fyn and dephosphorylates the GluN2B subunit of the NMDA receptor, whereas the protein kinase A phosphorylation of STEP61 inhibits the activity of the phosphatase (Pharmacol. Rev., 64, , p. 65). Previously, we found that ethanol activates Fyn in the dorsomedial striatum (DMS) leading to GluN2B phosphorylation, which, in turn, underlies the development of ethanol intake (J. Neurosci., 30, , p. 10187). Here, we tested the hypothesis that inhibition of STEP61 by ethanol is upstream of Fyn/GluN2B. We show that exposure of mice to ethanol increased STEP61 phosphorylation in the DMS, which was maintained after withdrawal and was not observed in other striatal regions. Specific knockdown of STEP61 in the DMS of mice enhanced ethanol-mediated Fyn activation and GluN2B phosphorylation, and increased ethanol intake without altering the level of water, saccharine, quinine consumption or spontaneous locomotor activity. Together, our data suggest that blockade of STEP61 activity in response to ethanol is sufficient for the activation of the Fyn/GluN2B pathway in the DMS. Being upstream of Fyn and GluN2B, inactive STEP61 in the DMS primes the induction of ethanol intake. We show that ethanol-mediated inhibition of STEP61 in the DMS leads to Fyn activation and GluN2B phosphorylation. (a) Under basal conditions, active STEP61 inhibits Fyn activity and dephosphorylates GluN2B. (b) Ethanol leads to the phosphorylation of STEP61 on a specific inhibitory site. The inhibition of STEP61 activity contributes to the activation of Fyn in response to ethanol, which, in turn, phosphorylates GluN2B. These molecular adaptations in the DMS promote ethanol drinking.
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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.