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

  1. Garcia Font, Nuria
Dirigée par:
  1. José Sánchez-Prieto Borja Directeur/trice
  2. María Jesús Oset Gasque Directeur/trice

Université de défendre: Universidad Complutense de Madrid

Fecha de defensa: 21 novembre 2019

Jury:
  1. Miguel Díaz Hernández President
  2. Jesús Miguel Pradillo Justo Secrétaire
  3. José María Solís Torralba Rapporteur
  4. David Bartolomé Martín Rapporteur
  5. Gertrudis Perea Parrilla Rapporteur

Type: Thèses

Résumé

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...