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Prenatal ethanol exposure and enkephalinergic neurotransmission

dc.creatorMéndez, Milagroses_ES
dc.creatorHernández-Fonseca, Karlaes_ES
dc.creatorAbate, Paulaes_ES
dc.date2019
dc.date.accessioned2023-05-10T18:10:21Z
dc.date.available2023-05-10T18:10:21Z
dc.date.issued2019
dc.identifierJC06SC23es_ES
dc.identifier.urihttp://repositorio.inprf.gob.mx/handle/123456789/7686
dc.identifier.urihttps://doi.org/10.1016/bs.vh.2019.05.005
dc.descriptionEndogenous opioids (enkephalins, endorphins and dynorphins) are small peptides that play a main role in pain perception and analgesia, as well as in alcohol (ethanol) reinforcement and reward. Alcohol reinforcement involves the ethanol-induced activation of the endogenous opioid system, a process that may augment the hedonic value and the reinforcing properties of the drug, which in turn increases substance consumption. Changes in opioidergic transmission may contribute to alcohol intoxication and to the neuroadaptive responses produced by the long-lasting exposure to ethanol. Opioidergic transmission may be altered by ethanol at distinct levels, including the expression of precursor mRNAs, biosynthesis and release of opioid peptides, as well as ligand binding to opioid receptors. In adult rats, β-endorphinergic and enkephalinergic transmission, through activation of mu and delta opioid receptors, mediate ethanol reinforcement and high alcohol drinking behavior. Prenatal ethanol exposure (PEE) selectively modifies Methionine-enkephalin (Met-enk) content in several brain regions of infant and adolescent rats, particularly those of the reward circuits. In preweanling rats, Met-enk content is decreased in the ventral tegmental area but is increased in the prefrontal cortex and the nucleus accumbens and other brain areas, as a consequence of a short and moderate ethanol exposure during late gestation. PEE also increases Met-enk levels in the prefrontal cortex and other brain regions of 30-day-old adolescent rats. These findings suggest that mesocorticolimbic enkephalins are essential in ethanol reinforcement in offspring, as previously reported in adult rats.es_ES
dc.formatPDFes_ES
dc.language.isoenges_ES
dc.publisherAcademic Presses_ES
dc.relation111:313-337
dc.rightsAcceso Cerradoes_ES
dc.titlePrenatal ethanol exposure and enkephalinergic neurotransmissiones_ES
dc.typeArtículoes_ES
dc.contributor.affiliationDepartamento de Neuroquímica, Subdirección de Investigaciones Clínicas, Instituto Nacional de Psiquiatría Ramón de la Fuente, Ciudad de México, México
dc.contributor.emailubach@imp.edu.mx
dc.relation.jnabreviadoVITAM HORM
dc.relation.journalVitamins and Hormones
dc.identifier.placeEstados Unidos
dc.date.published2019
dc.identifier.organizacionInstituto Nacional de Psiquiatría Ramón de la Fuente Muñiz
dc.identifier.eissn0083-6729
dc.identifier.doi10.1016/bs.vh.2019.05.005
dc.subject.kwAdolescents
dc.subject.kwAlcohol
dc.subject.kwDependence
dc.subject.kwEndogenous opioid system
dc.subject.kwEndorphins
dc.subject.kwEnkephalins
dc.subject.kwEthanol
dc.subject.kwInfants
dc.subject.kwPrenatal
dc.subject.kwReinforcement


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