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dc.contributor.otherUniversidad San Pablo-CEU. Facultad de Farmacia-
dc.creatorFernández Calle, Rosalía-
dc.creatorVicente Rodríguez, Marta-
dc.creatorPastor, Myriam-
dc.creatorGramage, Esther-
dc.creatorDi Geronimo Quintero, Bruno-
dc.creatorZapico Rodríguez, José María-
dc.creatorCoderch Boué, Claire-
dc.creatorPérez García, Carmen-
dc.creatorLasek, Amy W.-
dc.creatorPascual-Teresa Fernández, Beatriz de-
dc.creatorHerradón Gil-Gallardo, Gonzalo-
dc.date.accessioned2024-01-29T15:39:32Z-
dc.date.available2024-01-29T15:39:32Z-
dc.date.issued2018-07-15-
dc.identifier.citationFernández-Calle R, Vicente-Rodríguez M, Pastor M, Gramage E, Di Geronimo B, Zapico JM, et al. Pharmacological inhibition of Receptor Protein Tyrosine Phosphatase β/ζ (PTPRZ1) modulates behavioral responses to ethanol. Vol. 137, Neuropharmacology. 2018. p. 86-95.-
dc.identifier.issn0028-3908-
dc.identifier.urihttp://hdl.handle.net/10637/15216-
dc.description.abstractPleiotrophin (PTN) and Midkine (MK) are neurotrophic factors that are upregulated in the prefrontal cortex after alcohol administration and have been shown to reduce ethanol drinking and reward. PTN and MK are the endogenous inhibitors of Receptor Protein Tyrosine Phosphatase (RPTP) β/ζ (a.k.a. PTPRZ1, RPTPβ, PTPζ), suggesting a potential role for this phosphatase in the regulation of alcohol effects. To determine if RPTPβ/ζ regulates ethanol consumption, we treated mice with recently developed small-molecule inhibitors of RPTPβ/ζ (MY10, MY33-3) before testing them for binge-like drinking using the drinking in the dark protocol. Mice treated with RPTPβ/ζ inhibitors, particularly with MY10, drank less ethanol than controls. MY10 treatment blocked ethanol conditioned place preference, showed limited effects on ethanol-induced ataxia, and potentiated the sedative effects of ethanol. We also tested whether RPTPβ/ζ is involved in ethanol signaling pathways. We found that ethanol treatment of neuroblastoma cells increased phosphorylation of anaplastic lymphoma kinase (ALK) and TrkA, known substrates of RPTPβ/ζ. Treatment of neuroblastoma cells with MY10 or MY33-3 also increased levels of phosphorylated ALK and TrkA. However, concomitant treatment of neuroblastoma cells with ethanol and MY10 or MY33-3 prevented the increase in pTrkA and pALK. These results demonstrate for the first time that ethanol engages TrkA signaling and that RPTPβ/ζ modulates signaling pathways activated by alcohol and behavioral responses to this drug. The data support the hypothesis that RPTPβ/ζ might be a novel target of pharmacotherapy for reducing excessive alcohol consumption.en_EN
dc.language.isoenen_EN
dc.publisherElsevier-
dc.relation.ispartofNeuropharmacology-
dc.rightshttp://creativecommons.org/licenses/by/4.0/deed.es-
dc.subjectALKen_EN
dc.subjectTrkAen_EN
dc.subjectAlcohol use disorderen_EN
dc.subjectBinge-drinkingen_EN
dc.subjectPleiotrophinen_EN
dc.subjectMidkineen_EN
dc.titlePharmacological inhibition of Receptor Protein Tyrosine Phosphatase β/ζ (PTPRZ1) modulates behavioral responses to ethanolen_EN
dc.typeArtículoen_EN
dc.identifier.doi10.1016/j.neuropharm.2018.04.027-
dc.centroUniversidad San Pablo-CEU-
Aparece en las colecciones: Facultad de Farmacia




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