2026-06-28T04:47:34Zhttps://docta.ucm.es/rest/oai/request

oai:docta.ucm.es:20.500.14352/1049692025-08-28T17:05:45Zcom_20.500.14352_14col_20.500.14352_15

Flores, Andrea Moyano-Cires Ivanoff, Paula Viviana Sola Vendrell, Emma García Sánchez, José Manuel García Lobo, Jimena Frejo Moya, María Teresa Guerra Menéndez, Lucía Labajo González, Elena Lobo Lozano, Inés Abascal, Luisa Pino Sans, Javier Del 2024-06-14T16:41:26Z 2024-06-14T16:41:26Z 2023 Flores A, Moyano P, Sola E, García JM, García J, Frejo MT, et al. Bisphenol-A Neurotoxic Effects on Basal Forebrain Cholinergic Neurons In Vitro and In Vivo. Biology 2023;12:782. https://doi.org/10.3390/biology12060782. 10.3390/biology12060782 https://hdl.handle.net/20.500.14352/104969 https://doi.org/10.3390/biology12060782 https://www.mdpi.com/2079-7737/12/6/782 The widely used plasticizer bisphenol-A (BPA) is well-known for producing neurodegeneration and cognitive disorders, following acute and long-term exposure. Although some of the BPA actions involved in these effects have been unraveled, they are still incompletely known. Basal forebrain cholinergic neurons (BFCN) regulate memory and learning processes and their selective loss, as observed in Alzheimer’s disease and other neurodegenerative diseases, leads to cognitive decline. In order to study the BPA neurotoxic effects on BFCN and the mechanisms through which they are induced, 60-day old Wistar rats were used, and a neuroblastoma cholinergic cell line from the basal forebrain (SN56) was used as a basal forebrain cholinergic neuron model. Acute treatment of rats with BPA (40 µg/kg) induced a more pronounced basal forebrain cholinergic neuronal loss. Exposure to BPA, following 1- or 14-days, produced postsynaptic-density-protein-95 (PSD95), synaptophysin, spinophilin, and N-methyl-D-aspartate-receptor-subunit-1 (NMDAR1) synaptic proteins downregulation, an increase in glutamate content through an increase in glutaminase activity, a downregulation in the vesicular-glutamate-transporter-2 (VGLUT2) and in the WNT/β-Catenin pathway, and cell death in SN56 cells. These toxic effects observed in SN56 cells were mediated by overexpression of histone-deacetylase-2 (HDAC2). These results may help to explain the synaptic plasticity, cognitive dysfunction, and neurodegeneration induced by the plasticizer BPA, which could contribute to their prevention. eng https://creativecommons.org/licenses/by/4.0/ open access ATTRIBUTION 4.0 INTERNATIONAL Bisphenol-A Neurotoxic Effects on Basal Forebrain Cholinergic Neurons In Vitro and In Vivo journal article