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Could Perinatal Asphyxia Induce a Synaptopathy? New Highlights from an Experimental Model

dc.contributor.authorHerrera M.I.
dc.contributor.authorOtero-Losada M.
dc.contributor.authorUdovin L.D.
dc.contributor.authorKusnier C.
dc.contributor.authorKölliker-Frers R.
dc.contributor.authorDe Souza W.
dc.contributor.authorCapani F.
dc.date.accessioned2020-09-02T22:20:27Z
dc.date.available2020-09-02T22:20:27Z
dc.date.issued2017
dc.identifier10.1155/2017/3436943
dc.identifier.citation2017, , -
dc.identifier.issn20905904
dc.identifier.urihttps://hdl.handle.net/20.500.12728/4875
dc.descriptionBirth asphyxia also termed perinatal asphyxia is an obstetric complication that strongly affects brain structure and function. Central nervous system is highly susceptible to oxidative damage caused by perinatal asphyxia while activation and maturity of the proper pathways are relevant to avoiding abnormal neural development. Perinatal asphyxia is associated with high morbimortality in term and preterm neonates. Although several studies have demonstrated a variety of biochemical and molecular pathways involved in perinatal asphyxia physiopathology, little is known about the synaptic alterations induced by perinatal asphyxia. Nearly 25% of the newborns who survive perinatal asphyxia develop neurological disorders such as cerebral palsy and certain neurodevelopmental and learning disabilities where synaptic connectivity disturbances may be involved. Accordingly, here we review and discuss the association of possible synaptic dysfunction with perinatal asphyxia on the basis of updated evidence from an experimental model. © 2017 Mariá Inés Herrera et al.
dc.language.isoen
dc.publisherHindawi Limited
dc.titleCould Perinatal Asphyxia Induce a Synaptopathy? New Highlights from an Experimental Model
dc.typeReview


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