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

  1. Garcia Font, Nuria
Zuzendaria:
  1. José Sánchez-Prieto Borja Zuzendaria
  2. María Jesús Oset Gasque Zuzendaria

Defentsa unibertsitatea: Universidad Complutense de Madrid

Fecha de defensa: 2019(e)ko azaroa-(a)k 21

Epaimahaia:
  1. Miguel Díaz Hernández Presidentea
  2. Jesús Miguel Pradillo Justo Idazkaria
  3. José María Solís Torralba Kidea
  4. David Bartolomé Martín Kidea
  5. Gertrudis Perea Parrilla Kidea

Mota: Tesia

Laburpena

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...