dc.creator | Guevara Miranda, David Ladrón de | es |
dc.creator | Millón, Carmelo | es |
dc.creator | Rosell Valle, Cristina | es |
dc.creator | Pérez Fernández, Mercedes | es |
dc.creator | Missiroli, Michele | es |
dc.date.accessioned | 2017-08-16T08:42:23Z | |
dc.date.available | 2017-08-16T08:42:23Z | |
dc.date.issued | 2017 | |
dc.identifier.citation | Guevara Miranda, D.L.d., Millón, C., Rosell Valle, C., Pérez Fernández, M. y Missiroli, . (2017). Long-lasting memory deficits in mice withdrawn from cocaine are concomitant with neuroadaptations in hippocampal basal activity, GABAergic interneurons and adult neurogenesis. Disease Models and Mechanisms, 10 (3), 323-336. | |
dc.identifier.issn | 1754-8403 | es |
dc.identifier.uri | http://hdl.handle.net/11441/63786 | |
dc.description.abstract | Cocaine addiction disorder is notably aggravated by concomitant cognitive and emotional pathology that impedes recovery. We studied whether a persistent cognitive/emotional dysregulation in mice withdrawn from cocaine holds a neurobiological correlate within the hippocampus, a limbic region with a key role in anxiety and memory but that has been scarcely investigated in cocaine addiction research. Mice were submitted to a chronic cocaine (20 mg/kg/day for 12 days) or vehicle treatment followed by 44 drug-free days. Some mice were then assessed on a battery of emotional (elevated plus-maze, light/dark box, open field, forced swimming) and cognitive (object and place recognition memory, cocaine-induced conditioned place preference, continuous spontaneous alternation) behavioral tests, while other mice remained in their home cage. Relevant hippocampal features [basal c-Fos activity, GABA+, parvalbumin (PV)+ and neuropeptide Y (NPY)+ interneurons and adult neurogenesis (cell proliferation and immature neurons)] were immunohistochemically assessed 73 days after the chronic cocaine or vehicle protocol. The cocaine-withdrawn mice showed no remarkable exploratory or emotional alterations but were consistently impaired in all the cognitive tasks. All the cocaine-withdrawn groups, independent of whether they were submitted to behavioral assessment or not, showed enhanced basal c-Fos expression and an increased number of GABA+ cells in the dentate gyrus. Moreover, the cocaine-withdrawn mice previously submitted to behavioral training displayed a blunted experience-dependent regulation of PV+ and NPY+ neurons in the dentate gyrus, and neurogenesis in the hippocampus. Results highlight the importance of hippocampal neuroplasticity for the ingrained cognitive deficits present during chronic cocaine withdrawal. | es |
dc.format | application/pdf | es |
dc.language.iso | eng | es |
dc.publisher | Company of Biologists | es |
dc.relation.ispartof | Disease Models and Mechanisms, 10 (3), 323-336. | |
dc.rights | Attribution-NonCommercial-NoDerivatives 4.0 Internacional | * |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/4.0/ | * |
dc.subject | Neuropeptide Y | es |
dc.subject | Anxiety | es |
dc.subject | Parvalbumin | es |
dc.subject | Cell proliferation | es |
dc.subject | Behavior-induced neuroplasticity | es |
dc.title | Long-lasting memory deficits in mice withdrawn from cocaine are concomitant with neuroadaptations in hippocampal basal activity, GABAergic interneurons and adult neurogenesis | es |
dc.type | info:eu-repo/semantics/article | es |
dcterms.identifier | https://ror.org/03yxnpp24 | |
dc.type.version | info:eu-repo/semantics/publishedVersion | es |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | es |
dc.relation.publisherversion | http://dx.doi.org/ 10.1242/dmm.026682 | es |
dc.identifier.doi | 10.1242/dmm.026682 | es |
idus.format.extent | 17 p. | es |
dc.journaltitle | Disease Models and Mechanisms | es |
dc.publication.volumen | 10 | es |
dc.publication.issue | 3 | es |
dc.publication.initialPage | 323 | es |
dc.publication.endPage | 336 | es |