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Bisphenol A single and repeated treatment increases HDAC2, leading to cholinergic neurotransmission dysfunction and SN56 cholinergic apoptotic cell death through AChE variants overexpression and NGF/TrkA/P75NTR signaling disruption

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Moyano, Paula & Flores, Andrea & García, José Manuel & Anadon, María José & Frejo, María Teresa & Sola, Emma & Pelayo, Adela & del Pino, Javier & García Lobo, Jimena .Bisphenol A single and repeated treatment increases HDAC2, leading to cholinergic neurotransmission dysfunction and SN56 cholinergic apoptotic cell death through AChE variants overexpression and NGF/TrkA/P75NTR signaling disruption.

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Moyano, Paula & Flores, Andrea & García, José Manuel & Anadon, María José & Frejo, María Teresa & Sola, Emma & Pelayo, Adela & del Pino, Javier & García Lobo, Jimena. Bisphenol A single and repeated treatment increases HDAC2, leading to cholinergic neurotransmission dysfunction and SN56 cholinergic apoptotic cell death through AChE variants overexpression and NGF/TrkA/P75NTR signaling disruption.

https://hdl.handle.net/20.500.12080/25978
dc.contributor.author Moyano, Paula
dc.contributor.author Flores, Andrea
dc.contributor.author García, José Manuel
dc.contributor.author Anadon, María José
dc.contributor.author Frejo, María Teresa
dc.contributor.author Sola, Emma
dc.contributor.author Pelayo, Adela
dc.contributor.author del Pino, Javier
dc.contributor.author García Lobo, Jimena
dc.date.accessioned 2021-10-26T13:09:14Z
dc.date.available 2021-10-26T13:09:14Z
dc.date.created 2021-10-12
dc.identifier.uri https://hdl.handle.net/20.500.12080/25978
dc.description.abstract Bisphenol-A (BPA), a widely used plasticizer, induces cognitive dysfunctions following single and repeated exposure. Several studies, developed in hippocampus and cortex, tried to find the mechanisms that trigger and mediate these dysfunctions, but those are still not well known. Basal forebrain cholinergic neurons (BFCN) innervate hippocampus and cortex, regulating cognitive function, and their loss or the induction of cholinergic neurotransmission dysfunction leads to cognitive disabilities. However, no studies were performed in BFCN. We treated wild type or histone deacetylase (HDAC2), P75NTR or acetylcholinesterase (AChE) silenced SN56 cholinergic cells from BF with BPA (0.001 ¿M¿100 ¿M) with or without recombinant nerve growth factor (NGF) and with or without acetylcholine (ACh) for one- and fourteen days in order to elucidate the mechanisms underlying these effects. BPA induced cholinergic neurotransmission disruption through reduction of ChAT activity, and produced apoptotic cell death, mediated partially through AChE-S overexpression and NGF/TrkA/P75NTR signaling dysfunction, independently of cholinergic neurotransmission disruption, following one- and fourteen days of treatment. BPA mediates these alterations, in part, through HDAC2 overexpression. These data are relevant since they may help to elucidate the neurotoxic mechanisms that trigger the cognitive disabilities induced by BPA exposure, providing a new therapeutic approach. es_ES
dc.format application/pdf es_ES
dc.language eng es_ES
dc.rights CC-BY es_ES
dc.rights.uri http://creativecommons.org/licenses/by/4.0/deed.es es_ES
dc.subject Bisphenol A ,SN56 basal forebrain cholinergic neurons ,HDAC2, NGF ,P75NTR ,TrkA ,AChE ,ChAT es_ES
dc.title Bisphenol A single and repeated treatment increases HDAC2, leading to cholinergic neurotransmission dysfunction and SN56 cholinergic apoptotic cell death through AChE variants overexpression and NGF/TrkA/P75NTR signaling disruption es_ES
dc.type info:eu-repo/semantics/article es_ES
dc.rights.accessrights info:eu-repo/semantics/openAccess es_ES
dc.identifier.location N/A es_ES


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