Abstract
It is widely believed that activity-dependent synaptic plasticity is the basis for learning and memory. Both processes are dependent on new protein synthesis at the synapse. Here, we describe a mechanism how dendritic mRNAs are transported and subsequently translated at activated synapses. Furthermore, we present the players involved in the regulation of local dendritic translation upon neuronal stimulation and their molecular interplay that maintain local proteome homeostasis. Any dysregulation causes several types of neurological disorders including muscular atrophies, cancers, neuropathies, neurodegenerative, and cognitive disorders.
Highlights
It is widely believed that activity-dependent synaptic plasticity is the basis for learning and memory
It has been shown that components of the translational machinery, e.g., ribosomes, tRNAs, as well as translation initiation and elongation factors (Steward and Levy, 1982; Tiedge and Brosius, 1996; Sutton and Schuman, 2006), co-translational protein sorting organelles (Davis et al, 1987; Gardiol et al, 1999), the RNA-induced silencing complex (RISC) and microRNAs are all present at the synapse
These findings suggest that local translation can be regulated in a defined compartment and that this is dependent on synaptic activity
Summary
It is widely believed that activity-dependent synaptic plasticity is the basis for learning and memory. In this review we will first focus on recent evidence that supports a possible link between RNA transport and translational control of localized mRNAs as well as the necessity and importance of a tight translational regulation at the synapse. We analyze the recent evidences that RNA-binding proteins (RBPs) and miRNAs play an important role in translational control in neurons.
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