Fig. 2.

NO signalling in autism spectrum disorder (ASD). Schematic representation of NO involvement in ASD. Mutation in SHANK3 gene may cause imbalance in Ca⁺² homeostasis. Ca⁺² is responsible for intracellular NO production which leads to S-nitrosylation of many proteins. S-nitrosylation of calcineurin inhibited its phosphatase activity which leads to increased levels of phosphorylated (P) synapsin-1 and CREB. P-synapsin-1 increases vesicle mobilization and P-CREB increases the recruitment of transcriptional co-activators and cortical activity. S-nitrosylation of syntaxin1a, inhibited its binding with Munc-18 which ultimately leads to increased vesicle docking and fusion.