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Abstract
Synaptic plasticity mechanisms are usually discussed in terms of changes in synaptic strength. The capacity of excitatory synapses to rapidly modify the membrane expression of glutamate receptors in an activity-dependent manner plays a critical role in learning and memory processes by re-distributing activity within neuronal networks. Recent work has however also shown that functional plasticity properties are associated with a rewiring of synaptic connections and a selective stabilization of activated synapses. These structural aspects of plasticity have the potential to continuously modify the organization of synaptic networks and thereby introduce specificity in the wiring diagram of cortical circuits. Recent work has started to unravel some of the molecular mechanisms that underlie these properties of structural plasticity, highlighting an important role of signaling pathways that are also major candidates for contributing to developmental psychiatric disorders. We review here some of these recent advances and discuss the hypothesis that alterations of structural plasticity could represent a common mechanism contributing to the cognitive and functional defects observed in diseases such as intellectual disability, autism spectrum disorders and schizophrenia.
Highlights
Dendritic spines are the major site for excitatory transmission in the brain
While most research attention has usually focused on the functional aspects of synaptic plasticity and their key contribution to learning and memory mechanisms, work in the last decade has clearly demonstrated the importance of the associated structural rearrangements
In studies that we carried out to analyze the role of N-cadherin in structural plasticity, we found that an extracellular mutant of N-cadherin strongly affects the life time of dendritic spines and that it prevents activity-mediated spine stabilization (Mendez et al, 2010a)
Summary
Dendritic spines are the major site for excitatory transmission in the brain. They are usually contacted by en passant presynaptic terminals and most often surrounded by astrocytic processes, forming complex structures that dysplay a high degree of functional and structural plasticity. Based on this type of results, one can propose that changes in spine turnover and changes in spine stability represent two key mechanisms associated with memory that could account for some of its antinomic properties: the capacity to learn, which requires adaptation of existing networks, and the capacity to retain information, which requires to maintain important functional circuits (Caroni et al, 2012; see Figure 1).
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