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Acylethanolamides and endocannabinoid signaling system in dorsal striatum of rats exposed to perinatal asphyxia

dc.contributor.authorHolubiec M.I.
dc.contributor.authorRomero J.I.
dc.contributor.authorBlanco E.
dc.contributor.authorTornatore T.L.
dc.contributor.authorSuarez J.
dc.contributor.authorRodríguez de Fonseca F.
dc.contributor.authorGaleano P.
dc.contributor.authorCapani F.
dc.date.accessioned2020-09-02T22:20:31Z
dc.date.available2020-09-02T22:20:31Z
dc.date.issued2017
dc.identifier10.1016/j.neulet.2017.05.068
dc.identifier.citation653, , 269-275
dc.identifier.issn03043940
dc.identifier.urihttps://hdl.handle.net/20.500.12728/4906
dc.descriptionEndocannabinoids (eCBs) and acylethanolamides (AEs) have lately received more attention due to their neuroprotective functions in neurological disorders. Here we analyze the alterations induced by perinatal asphyxia (PA) in the main metabolic enzymes and receptors of the eCBs/AEs in the dorsal striatum of rats. To induce PA, we used a model developed by Bjelke et al. (1991). Immunohistochemical techniques were carried out to determine the expression of neuronal and glial markers (NeuN and GFAP), eCBs/AEs synthesis and degradation enzymes (DAGLα, NAPE-PLD and FAAH) and their receptors (CB1 and PPARα). We found a decrease in NAPE-PLD and PPARα expression. Since NAPE-PLD and PPARα take part in the production and reception of biochemical actions of AEs, such as oleoylethanolamide, these results may suggest that PA plays a key role in the regulation of this system. These data agree with previous results obtained in the hippocampus and encourage us to develop further studies using AEs as potential neuroprotective compounds. © 2017 Elsevier B.V.
dc.language.isoen
dc.publisherElsevier Ireland Ltd
dc.subjectCB1
dc.subjectDAGLα
dc.subjectDorsal striatum
dc.subjectNAPE-PLD
dc.subjectPerinatal asphyxia
dc.subjectPPARα
dc.subjectacylethanolamide derivative
dc.subjectcannabinoid receptor
dc.subjectendocannabinoid
dc.subjectglial fibrillary acidic protein
dc.subjectn oleoylethanolamine
dc.subjectneuron specific nuclear protein
dc.subjectperoxisome proliferator activated receptor alpha
dc.subjectunclassified drug
dc.subjectcannabinoid 1 receptor
dc.subjectendocannabinoid
dc.subjectlipoprotein lipase
dc.subjectNAPE-PLD protein, rat
dc.subjectperoxisome proliferator activated receptor alpha
dc.subjectphospholipase D
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectanimal tissue
dc.subjectArticle
dc.subjectcontrolled study
dc.subjectdorsal striatum
dc.subjectenzyme degradation
dc.subjectimmunohistochemistry
dc.subjectnonhuman
dc.subjectperinatal asphyxia
dc.subjectpriority journal
dc.subjectprotein expression
dc.subjectrat
dc.subjectsignal transduction
dc.subjectanimal
dc.subjectcorpus striatum
dc.subjectdisease model
dc.subjectmetabolism
dc.subjectnewborn
dc.subjectnewborn hypoxia
dc.subjectphysiology
dc.subjectSprague Dawley rat
dc.subjectAnimals
dc.subjectAnimals, Newborn
dc.subjectAsphyxia Neonatorum
dc.subjectCorpus Striatum
dc.subjectDisease Models, Animal
dc.subjectEndocannabinoids
dc.subjectLipoprotein Lipase
dc.subjectPhospholipase D
dc.subjectPPAR alpha
dc.subjectRats
dc.subjectRats, Sprague-Dawley
dc.subjectReceptor, Cannabinoid, CB1
dc.subjectSignal Transduction
dc.titleAcylethanolamides and endocannabinoid signaling system in dorsal striatum of rats exposed to perinatal asphyxia
dc.typeArticle


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