Hebbian synaptic plasticity, such as hippocampal long-term potentiation (LTP), is thought to be impor- tant for particular types of learning and memory. It involves changes in the expression and activity of a large array of proteins, including cell adhesion molecules. The integrin class of cell adhesion molecules has been extensively studied in this respect, and appear to have a defined role in consolidating both struc- tural and functional changes brought about by LTP. With the use ofintegrin inhibitors, it has been possible to identify a critical time window ofseveral minutes after LTP induction for the participation ofintegrins in LTP. Altering the interactions of integrins with their ligands during this time compromises structural changes involving actin polymerisation and spine enlargement that could be required for accommodat- ing new AMPA receptors (AMPARs). After this critical window of structural remodelling and plasticity, integrins “lock-in” and stabilise the morphological changes, conferring the requisite longevity for LTP. Genetic manipulations targeting integrin subtypes have helped identify the specific integrin subunits involved in LTP and correlate alterations in plasticity with behavioural deficits. Moreover, recent studies have implicated integrins in AMPAR trafficking and glycine receptor lateral diffusion, highlighting their multifaceted functions at the synapse.

A stabilizing influence: Integrins in regulation of synaptic plasticity

Cingolani L;
2011-01-01

Abstract

Hebbian synaptic plasticity, such as hippocampal long-term potentiation (LTP), is thought to be impor- tant for particular types of learning and memory. It involves changes in the expression and activity of a large array of proteins, including cell adhesion molecules. The integrin class of cell adhesion molecules has been extensively studied in this respect, and appear to have a defined role in consolidating both struc- tural and functional changes brought about by LTP. With the use ofintegrin inhibitors, it has been possible to identify a critical time window ofseveral minutes after LTP induction for the participation ofintegrins in LTP. Altering the interactions of integrins with their ligands during this time compromises structural changes involving actin polymerisation and spine enlargement that could be required for accommodat- ing new AMPA receptors (AMPARs). After this critical window of structural remodelling and plasticity, integrins “lock-in” and stabilise the morphological changes, conferring the requisite longevity for LTP. Genetic manipulations targeting integrin subtypes have helped identify the specific integrin subunits involved in LTP and correlate alterations in plasticity with behavioural deficits. Moreover, recent studies have implicated integrins in AMPAR trafficking and glycine receptor lateral diffusion, highlighting their multifaceted functions at the synapse.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11368/2938930
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