Carbonic anhydrase activation enhances object recognition memory in mice through phosphorylation of the extracellular signal-regulated kinase in the cortex and the hippocampus

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dc.contributor.authorCanto de Souza, Lucas [UNESP]
dc.contributor.authorProvensi, Gustavo
dc.contributor.authorVullo, Daniela
dc.contributor.authorCarta, Fabrizio
dc.contributor.authorScozzafava, Andrea
dc.contributor.authorCosta, Alessia
dc.contributor.authorSchmidt, Scheila Daiane
dc.contributor.authorPassani, Maria Beatrice
dc.contributor.authorSupuran, Claudiu T.
dc.contributor.authorBlandina, Patrizio
dc.contributor.institutionUniversità degli Studi di Firenze
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.date.accessioned2018-12-11T16:46:29Z
dc.date.available2018-12-11T16:46:29Z
dc.date.issued2017-05-15
dc.description.abstractRats injected with by D-phenylalanine, a carbonic anhydrase (CA) activator, enhanced spatial learning, whereas rats given acetazolamide, a CA inhibitor, exhibited impairments of fear memory consolidation. However, the related mechanisms are unclear. We investigated if CAs are involved in a non-spatial recognition memory task assessed using the object recognition test (ORT). Systemic administration of acetazolamide to male CD1 mice caused amnesia in the ORT and reduced CA activity in brain homogenates, while treatment with D-phenylalanine enhanced memory and increased CA activity. We provided also the first evidence that D-phenylalanine administration rapidly activated extracellular signal-regulated kinase (ERK) pathways, a critical step for memory formation, in the cortex and the hippocampus, two brain areas involved in memory processing. Effects elicited by D-phenylalanine were completely blunted by co-administration of acetazolamide, but not of 1-N-(4-sulfamoylphenyl-ethyl)-2,4,6-trimethylpyridinium perchlorate (C18), a CA inhibitor that, differently from acetazolamide, does not cross the blood brain barrier. Our results strongly suggest that brain but not peripheral CAs activation potentiates memory as a result of ERK pathway enhanced activation.en
dc.description.affiliationDipartimento di Neuroscienze Psicologia Area del Farmaco e Salute del Bambino Università degli Studi di Firenze
dc.description.affiliationDipartimento di Chimica 'Ugo Schiff' Università degli Studi di Firenze
dc.description.affiliationDipartimento di Scienze della Salute Università degli Studi di Firenze
dc.description.affiliationFaculdade de Ciências Farmacêuticas Universidade Estadual Paulista-UNESP
dc.description.affiliationUnespFaculdade de Ciências Farmacêuticas Universidade Estadual Paulista-UNESP
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.description.sponsorshipFondazione Umberto Veronesi
dc.description.sponsorshipIdCNPq: 201511/2014-2
dc.format.extent148-156
dc.identifierhttp://dx.doi.org/10.1016/j.neuropharm.2017.03.009
dc.identifier.citationNeuropharmacology, v. 118, p. 148-156.
dc.identifier.doi10.1016/j.neuropharm.2017.03.009
dc.identifier.file2-s2.0-85016087223.pdf
dc.identifier.issn1873-7064
dc.identifier.issn0028-3908
dc.identifier.scopus2-s2.0-85016087223
dc.identifier.urihttp://hdl.handle.net/11449/169570
dc.language.isoeng
dc.relation.ispartofNeuropharmacology
dc.relation.ispartofsjr2,043
dc.rights.accessRightsAcesso aberto
dc.sourceScopus
dc.subject1-N-(4-sulfamoylphenyl-ethyl)-2,4,6-Trimethylpyridinium perchlorate
dc.subjectAcetazolamide
dc.subjectD-phenylalanine
dc.titleCarbonic anhydrase activation enhances object recognition memory in mice through phosphorylation of the extracellular signal-regulated kinase in the cortex and the hippocampusen
dc.typeArtigo

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