Ricerc@Sapienza

NMDA receptors (NMDARs) are glutamate-gated ion channels involved in excitatory synaptic transmission and in others physiological processes such as synaptic plasticity and development. The overload of Ca2+ ions through NMDARs, caused by an excessive activation of receptors, leads to excitotoxic neuronal cell death. For this reason, the reduction of Ca2+ flux through NMDARs has been a central focus in finding therapeutic strategies to prevent neuronal cell damage. Extracellular H+ are allosteric modulators of NMDARs.

Mutations in fused in sarcoma (FUS) cause amyotrophic lateral sclerosis (ALS). FUS is a multifunctional protein involved in the
biogenesis and activity of several types of RNAs, and its role in the pathogenesis of ALS may involve both direct effects of
disease-associated mutations through gain- and loss-of-function mechanisms and indirect effects due to the cross talk between
different classes of FUS-dependent RNAs. To explore how FUS mutations impinge on motor neuron-specific RNA-based