Topic: NLGN3-R451C

Autistic spectrum disorder (ASD) has been associated with genetic alterations of synaptic proteins such as the point mutation R451C in neuroligin 3 (NLGN3), a postsynaptic adhesion molecule located at both excitatory and inhibitory synapses. By exploiting the transgenic NLGN3-R451C knock-in (KI) mice, an animal model of ASD, we investigated this mutation in the coordination of excitatory and inhibitory synaptic plasticity. In hippocampal primary cultures, while the NLGN3-R451C protein was less expressed in KI mice with respect to WT, the molecular and functional properties of basal excitatory

The ability to predict the consequences of behavior and the flexibility to modify behavior based on outcome and changes in reward contingency is critical for not only survival but also for maximizing reward. Acquisition and consolidation of social reward contingencies is essential for both prediction and flexibility. During the presentation of emotionally charged stimuli, the amygdala encodes the salience of social stimuli as ensembles of neurons with individual stimuli preferences. Correct evaluation of prediction errors, defined as the difference between expectation and result, is critical f