Control presináptico por receptores acoplados a proteínas G, GPCRs, en un ratón modelo del síndrome X frágil

  1. Garcia Font, Nuria
Dirigida por:
  1. José Sánchez-Prieto Borja Director/a
  2. María Jesús Oset Gasque Director/a

Universidad de defensa: Universidad Complutense de Madrid

Fecha de defensa: 21 de noviembre de 2019

Tribunal:
  1. Miguel Díaz Hernández Presidente/a
  2. Jesús Miguel Pradillo Justo Secretario/a
  3. José María Solís Torralba Vocal
  4. David Bartolomé Martín Vocal
  5. Gertrudis Perea Parrilla Vocal

Tipo: Tesis

Resumen

Fragile X syndrome (FXS) is the most common inherited intellectual disability and it is associated with multiple behavioral alterations, including cognitive deficits, hyperactivity, anxiety and deficits in social behavior. In FXS, the Fmr1 gene that encodes the fragile mental retardation protein (FMRP) is silenced. FMRP modulates gene expression through changes in the stability and transport of its mRNA targets. When FMRP is absent the expression of many postsynaptic proteins is altered as well as postsynaptic long-term forms of plasticity. FMRP is also found in axons and presynaptic nerve terminals and mRNA targets encoding for presynaptic proteins were identified...