Topic: silent synapses

CLN3 is a lysosomal membrane protein whose precise function is not yet known. Recent studies propose divergent functions for CLN3; as a vesicular trafficking hub or its role in glycerophosphodiester (GPD) efflux from lysosomes. The role of CLN3 in the neurons and at the synapse remains elusive. Mutations in CLN3 gene cause Juvenile Neuronal Ceroid Lipofuscinosis (JNCL), a condition associated with learning impairments and memory deficits in affected children. Using CLN3Δex7/8 mouse model, we investigated the impact of CLN3 loss at synapses. Analysis of synaptic transmission revealed a signific

Repetitive cocaine exposure induces the generation of silent synapses in the nucleus accumbens, characterized by the presence of NMDA receptors and absence of AMPA receptors, hindering fast synaptic transmission (Huang et al, 2009). While typically abundant during early postnatal development, cocaine triggers the de novo generation of silent synapses in the adult brain, thereby establishing new synaptic connections within an already refined circuit (Huang et al, 2009; Huang et al, 2015). During withdrawal, some silent synapses undergo unsilencing by incorporating AMPARs, which crucially contri