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dc.contributor.authorMoreno-Fernández, Román D.
dc.contributor.authorNieto-Quero, Andrea
dc.contributor.authorGómez-Salas, Francisco Javier
dc.contributor.authorTabbai-Amal, Sara
dc.contributor.authorGarcía-Fernández, María Inmaculada 
dc.contributor.authorChun, Jerold
dc.contributor.authorPedraza-Benítez, María del Carmen 
dc.contributor.authorRosell-del-Valle, Cristina
dc.contributor.authorPérez-Martín, Margarita 
dc.contributor.authorRodriguez-de-Fonseca, Fernando
dc.contributor.authorEstivill-Torrús, Guillermo
dc.contributor.authorSantín-Núñez, Luis Javier 
dc.date.accessioned2018-07-16T11:59:51Z
dc.date.available2018-07-16T11:59:51Z
dc.date.created2018-07-08
dc.date.issued2018-07-16
dc.identifier.urihttps://hdl.handle.net/10630/16284
dc.description.abstractLPA1 receptor is one of the six characterized G protein-coupled receptors (LPA1-6) through which lysophosphatidic acid acts as an intercellular signalling molecule. It has been recently proposed that this receptor has a key role in controlling depression-like behaviours and in the detrimental consequences of stress. Here, we sought to establish the involvement of the LPA1 receptor in brain activity after an acute stressor. To this end, we examined behavioural despair in mice with a constitutive depletion of the LPA1 receptor (maLPA1-null mice), wild-type mice and mice receiving one single icv dose of the LPA1 receptor antagonist Ki16425 or vehicle. Furthermore, the expression of c-Fos protein in stress-related brain areas and the corticosterone response following acute stress were examined. Our data indicated that, contrary to the knockout model, the antagonism of the LPA1 receptor significantly increased immobility in the Forced Swim Test. However, latency to first immobility was reduced in both experimental conditions. Immunohistochemistry studies revealed an increased in activity in key limbic structures such as medial prefrontal cortex in both the LPA1 antagonist-treated mice and maLPA1-null mice, with an interesting opposed effect on hippocampal activity. Following acute stress, the sole infusion of Ki16425 in the cerebral ventricle increased corticosterone levels. In conclusion, the alteration of LPA1 receptor function, through both genetic deletion or pharmacological antagonism, is involved in behavioural despair and hyperactivity of brain stress systems, thus contributing to explore specific susceptibility mechanisms of stress as targets for therapeutic recovery.en_US
dc.description.sponsorshipFunding by the Andalusian Ministry of Economy, Innovation, Science and Employment (SEJ1863) and the Spanish Ministry of Education, Culture and Sports ( PSI2017 - 83408 - P). Authors RD. M-F and A. N-Q hold a Grant of the Spanish Ministry of Education, Culture and Sports (FPU14/01610 and FPU16/05308, respectively). Author S.T. holds a Grant of the Andalusian Ministry of Economy, Innovation, Science and Employment C. R. (FPDI 2016); Andalucía Tech. I Plan Propio de Investiga ción y Transferencia de la Universidad de Málaga. Universidad de Málaga. Campus de Excelencia Internacional Andalucía Techen_US
dc.language.isoengen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectNeurociencias - Congresosen_US
dc.subject.otherStress coping behaviouren_US
dc.subject.otherBrain connectivity LPA1 receptoren_US
dc.subject.otherDepressionen_US
dc.subject.otherAnimal modelsen_US
dc.titleStress coping behaviour, brain connectivity and LPA1 receptor: similarities and differences between the genetic and the pharmacological approachen_US
dc.typeinfo:eu-repo/semantics/conferenceObjecten_US
dc.centroFacultad de Psicología y Logopediaen_US
dc.relation.eventtitle11th FENS FORUM OF NEUROSCIENCEen_US
dc.relation.eventplaceBERLÍN (ALEMANIA)en_US
dc.relation.eventdate07/07/2018-11/07/2018en_US


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