Person:
Díaz Plaza, María Jesús

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First Name
María Jesús
Last Name
Díaz Plaza
Affiliation
Universidad Complutense de Madrid
Faculty / Institute
Veterinaria
Department
Area
Toxicología
Identifiers
UCM identifierDialnet ID

Search Results

Now showing 1 - 7 of 7
  • Publication
    Guía de prácticas y seminarios de Fundamentos de Toxicología
    (2021) Ramos Alonso, Eva; Del Pino Sans, Javier; Romero Martínez, Manuel Alejandro; Díaz Plaza, María Jesús; Frejo Moya, María Teresa; Moyano-Cires Ivanoff, Paula Viviana
  • Publication
    Aprendizaje flexible y personalizado para atender la diversidad en el aula, mediante la gamificación, a través del uso integrado de un sistema virtual de respuesta en el aula para dispositivos móviles con acceso a internet y una aplicación de screencasting
    (2018-06-01) Del Pino Sans, Javier; Martin Sopeña, Alejandra; López Salas, Alejandra; De Frías González, Mariano; Zeballos Deza, Gabriela; Moyano-Cires Ivanoff, Paula; García Sánchez, José Manuel; Frejo Moya, María Teresa; Anadón Baselga, María José; Capó Martí, Miguel Andrés; Díaz Plaza, María Jesús; Lobo Alonso, Margarita; Garcia Lobo, Jimena; Pelayo Alarcon, Adela; Blanco Caneda, Maria Luisa; Peligros Gómez, Isabel; Menarguez Palanca, Javier; López Varela, María del Carmen; Medina Ortega, Luis; Rodriguez Gil, Yolanda; Agra Pujol, Carolina; Fernández Aceñero, María Jesús; Sola Vendrell, Emma
  • Publication
    Guía de Prácticas de Laboratorio y seminarios de Toxicología Veterinaria
    (2021) Ramos Alonso, Eva; Del Pino Sans, Javier; Romero Martínez, Manuel Alejandro; Díaz Plaza, María Jesús; Frejo Moya, María Teresa; Moyano-Cires Ivanoff, Paula Viviana
  • Publication
    Guía de Prácticas de Laboratorio y seminarios de Toxicología de los Alimentos
    (2021) Moyano-Cires Ivanoff, Paula Viviana; Del Pino Sans, Javier; Romero Martínez, Manuel Alejandro; Díaz Plaza, María Jesús; Frejo Moya, María Teresa; Ramos Alonso, Eva
  • Publication
    Aprendizaje personalizado para facilitar la inserción en el mercado laboral, mediante la gamificación, a través del uso integrado de mundos y sistemas virtuales de respuesta en el aula para dispositivos móviles con acceso a internet
    (2019-06-03) Del Pino Sans, Javier; Moyano-Cires Ivanoff, Paula Viviana; Anadón Baselga, María José; Capó Martí, Miguel Andrés; Pelayo Alarcon, Adela; Sola Vendrell, Emma; De Frías González, Mariano; García Sánchez, José Manuel; Sanjuán López, Javier; Mourin Moral, Francisco Javier; Blanco Caneda, María Luisa; Díaz Plaza, María Jesús; Rojas Lopez, Francisco Javier; Frejo Moya, María Teresa; Lobo Alonso, Margarita; García Lobo, Jimena; Ruiz Fernandez, Matilde
    Integración de una aplicación informática propia como sistema de respuesta (clicker) y una aplicación de entorno simulado para facilitar la evaluación continúa de forma personalizada, aumentar la motivación y rendimiento a bajo coste.
  • Publication
    Cadmium induced ROS alters M1 and M3 receptors, leading to SN56 cholinergic neuronal loss, through AChE variants disruption
    (Elsevier, 2018-02-01) Moyano-Cires Ivanoff, Paula Viviana; De Frias, Mariano; Lobo Alonso, Margarita; Anadón Baselga, María José; Sola Vendrell, Emma; Pelayo Alarcón, Adela; Díaz Plaza, María Jesús; Frejo Moya, María Teresa; Pino Sans, Javier Del
    Cadmium, an environmental neurotoxic compound, produces cognitive disorders, although the mechanism remains unknown. Previously, we described that cadmium induces a more pronounced cell death on cholinergic neurons from basal forebrain (BF). This effect, partially mediated by M1 receptor blockade, triggering it through AChE splices variants alteration, may explain cadmium effects on learning and memory processes. Cadmium has been also reported to induce oxidative stress generation leading to M2 and M4 muscarinic receptors alteration, in hippocampus and frontal cortex, which are necessary to maintain cell viability and cognitive regulation, so their alteration in BF could also mediate this effect. Moreover, it has been reported that antioxidant treatment could reverse cognitive disorders, muscarinic receptor and AChE variants alterations induced by cadmium. Thus, we hypothesized that cadmium induced cell death of BF cholinergic neurons is mediated by oxidative stress generation and this mechanism could produce this effect, in part, through AChE variants altered by muscarinic receptors disruption. To prove this, we evaluated in BF SN56 cholinergic neurons, whether cadmium induces oxidative stress and alters muscarinic receptors, and their involvement in the induction of cell death through alteration of AChE variants. Our results show that cadmium induces oxidative stress, which mediates partially the alteration of AChE variants and M2 to M4 muscarinic receptors expression and blockage of M1 receptor. In addition, cadmium induced oxidative stress generation by M1 and M3 receptors alteration through AChE variants disruption, leading to cell death. These results provide new understanding of the mechanisms contributing to cadmium harmful effects on cholinergic neurons.
  • Publication
    Primary hippocampal neuronal cell death induction after acute and repeated paraquat exposures mediated by AChE variants alteration and cholinergic and glutamatergic transmission disruption
    (Elsevier, 2017-09-11) Pino Sans, Javier Del; Moyano-Cires Ivanoff, Paula Viviana; Gómez Díaz, Gloria; Anadón Baselga, María José; Díaz Plaza, María Jesús; García Sánchez, José Manuel; Lobo Alonso, Margarita; Pelayo Alarcón, Adela; Sola Vendrell, Emma; Frejo Moya, María Teresa
    Paraquat (PQ) is a widely used non-selective contact herbicide shown to produce memory and learning deficits after acute and repeated exposure similar to those induced in Alzheimer's disease (AD). However, the complete mechanisms through which it induces these effects are unknown. On the other hand, cholinergic and glutamatergic systems, mainly in the hippocampus, are involved on learning, memory and cell viability regulation. An alteration of hippocampal cholinergic or glutamatergic transmissions or neuronal cell loss may induce these effects. In this regard, it has been suggested that PQ may induce cell death and affect cholinergic and glutamatergic transmission, which alteration could produce neuronal loss. According to these data, we hypothesized that PQ could induce hippocampal neuronal loss through cholinergic and glutamatergic transmissions alteration. To prove this hypothesis, we evaluated in hippocampal primary cell culture, the PQ toxic effects after 24h and 14 consecutive days exposure on neuronal viability and the cholinergic and glutamatergic mechanisms related to it. This study shows that PQ impaired acetylcholine levels and induced AChE inhibition and increased CHT expression only after 14days exposure, which suggests that acetylcholine levels alteration could be mediated by these actions. PQ also disrupted glutamate levels through induction of glutaminase activity. In addition, PQ induced, after 24h and 14days exposure, cell death on hippocampal neurons that was partially mediated by AChE variants alteration and cholinergic and gultamatergic transmissions disruption. Our present results provide new view of the mechanisms contributing to PQ neurotoxicity and may explain cognitive dysfunctions observed after PQ exposure.