Jump Main Menu. Go directly to the main content

Sección de idiomas

EN

Fin de la sección de idiomas

Sección de utilidades

Calendar

Fin de la sección de utilidades

Secondary menu End of secondary menu

Research projects

Start of main content

Synaptogenesis induced by PI3K in memory processes

14th national competition for scientific and technical research

Molecular memory mechanisms

Senior Researcher : Ángel José Acebes Vindel

Research Centre or Institution : Instituto Cajal. CSIC. Madrid.

Abstract

Information transmission in the nervous system takes place in specialised contact areas between neurons called synapses. Synapses are dynamic structures that undergo development and activity-dependent changes. When the brain receives a stimulus or makes an association to create a memory, the functional state and, eventually, number of synapses change. However, during the ageing process, the brain gradually loses synapses, causing loss of cognitive faculties and memory. Identifying the mechanisms that control the number of synaptic contacts is, therefore, essential to understanding the pathological mechanisms that cause their loss, in addition to the mechanisms that enable memory to be created. Our work at the Cajal Institute of Madrid has revealed that the activation levels of the phosphoinositide 3-kinase (PI3K) protein regulate the number of synapses in the neurons of the insect /Drosophila melanogaster/, in human neuroblastoma cells and, finally, in cultured rat hypocamp cells, in a study carried out in collaboration with Dr. Miguel Morales at the IDIBAPS (Agusto Pi I Sunyer Biomedical Research Institute) in Barcelona. Overall, said results demonstrate that the synaptic pathway of PI3K is conserved in mammals, including humans. Our current project is aimed at studying the effects of PI3K in depth under experimental conditions that reproduce certain types of memory disorders, pathological neurodegeneration and ageing.

  • Activities related
  • Projects related
  • News related
  • Publications related

see all

End of main content