FMRP y las neuroliginas: la influencia de la actividad sensorial en las dinámicas del neurodesarrollo

In the critical period of development, occurring in postnatal stages,established synapses are remodeled. This process is dependent on theelectrical activity generated by the input of sensory stimuli that organismsexperience. The Fragile X mental retardation protein (FMRP) is amRNA translational regulatory protein that participates in the synapsesremodeling process, during this period. Failures in its function coincidewith the appearance of immature dendritic spines, overabundant neuralcircuits, and loss of plasticity. Neuroligins, for their part, are postsynapticneuronal adhesion proteins that assist dendritic specialization and maturation, and their mutation coincides with alterationsin synaptic transmission. FMRP and neuroligins areproteins regulated by sensory experience and necessaryfor of synaptic elimination and maturation processes,respectively. Failures in its expression are related toFragile X syndrome and Autism Spectrum Disordersthat can cause significant cognitive and behavioralproblems. In this review we examine the main findingson these proteins, their relationship, and their activity-dependent modulation through development. In addition,we highlight Drosophila melanogaster as a model organismfor emerging research in this field.