Inhibitory synaptic plasticity

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

…have been reported to recruit distinct synaptic plasticity mechanisms. However, it remains unknown whether and how Fos- and Npas4-mediated synaptic plasticity support memory consolidation. Here we provide experimental and computational evidence that Fos+ and Npas4+ neuronal ensembles coordinate different excitatory and inhibitory synaptic plasticity mechanisms to promote memory consolidat

Episodic memories are encoded by sparse populations of neurons activated during an experience. These neural ensembles constitute memory engrams that are both necessary and sufficient for inducing recall even long after memory acquisition. This suggests that following encoding, engrams are stabilized to support reliable memory retrieval. However, little is known about the temporal evolution of engrams over the course of memory consolidation or how it impacts mnemonic properties. Here we employed computational and experimental approaches to examine how the composition and selectivity of engrams