• Título:  TRAUMATIC BRAIN INJURY-INDUCED ALTERATIONS IN ADULT HIPPOCAMPAL NEUROGENESIS
• Autor:  DURÁ ESTEVE, IRENE
• Universidad:  Universidad del País Vasco/Euskal Herriko Unibertsitatea
• Departamento:  Neurociencias
• Fecha de Lectura:  20/01/2023
• Mención Europeo / Mención Internacional: concedido
• Programa de doctorado:  Programa de Doctorado en Neurociencias por la Universidad de A Coruña; la Universidad de Castilla-La Mancha; la Universidad del País Vasco/Euskal Herriko Unibertsitatea; la Universidad Pablo de Olavide y la Universidad Rovira i Virgili
• Dirección: 
  • PINEDA MARTÍ JOSÉ RAMÓN (DIRECTOR)
  • ENCINAS PEREZ, JUAN MANUEL (DIRECTOR)
• Tribunal: 
  • ORTEGA DE LA O, FELIPE (PRESIDENTE)
  • IBARRETXE BILBAO, GASKON (SECRETARIO)
  • RHINER, CHRISTA (VOCAL)
• Descriptores: 
  • NEUROFISIOLOGIA HUMANA
• Localización:  REPOSITORIO INSTITUCIONAL E.H.U./U.P.V.
• http://hdl.handle.net/10810/59617
• Resumen:
  Several important cognitive functions affected by traumatic brain injury (TBI) depend on the hippocampus, which harnesses several forms of neural plasticity, among them adult neurogenesis, the generation of new neurons throughout life. Adult hippocampal neurogenesis is a process involved in memory, learning and control of anxiety, cognitive functions which result impaired after TBI. We hypothesize that TBI induces fast and long-term changes in both neural stem cells (NSCs) and newborn neurons which could subsequently alter hippocampal and brain functioning. Using a model of controlled cortical impact (CCI) we have found that TBI has a dual effect on neurogenesis: In the short term (up to two months) it causes an increase in the number of newborn neurons but with aberrant migration, increased soma size and altered electrophysiological properties; in the long term, neurogenesis resultsimpaired by a reduction in the number of immature neurons. We also suggest that the alteration in the expression of Rho Family GTPase 2 (Rnd2) could be causing some of the morphological changes in the immature neurons as well as their aberrant migration and thus could be a target to prevent TBI-induced aberrant neurogenesis, a hypothesis that we are currently investigating at the cellular level. In addition, we have found that NSCs get activated in higher numbers early after TBI, a result that could explain the later reduction in neurogenesis.