The brain's ability to store and process memory for learning and for cognition is determined by synaptic plasticity. This process is defined as the ability of synapses to adapt with structural and/or functional changes to both internal and external stimuli. Two of the most studied forms of plasticity are long-term potentiation (LTP) and long-term depression (LTD). These plastic changes can be very diverse: from structural changes to adapt to possible damage, the activation or inhibition of metabolic/signaling pathways, the silencing or activation of genes, the formation and trimming of synapses, or the modification of existing synapses by endo- or exocytosis of membrane receptors and their adjacent components. These processes do not act independently. For example, changes at the genetic and epigenetic levels can lead to variations in the traffic of receptors to synapses. It is clear that the trafficking of AMPA receptors (AMPARs) is an important mechanism in both LTP and LTD. Finally, dysfunction of AMPAR plasticity is directly linked to symptoms in neurological and psychiatric disorders. Therefore, it is important to understand mechanisms involved in the plastic change of AMPARs.

The aim of this Research Topic (research articles and reviews) is to provide knowledge that helps clarify the following points:

1. Regulation of the expression and trafficking of AMPARs

2. Genetic and epigenetic remodeling of AMPAR plasticity

3. Novel techniques for examining the plasticity of AMPAR

4. Role of AMPAR plasticity in neurological and psychiatric disorders

5. Role of glia on the expression and function of AMPAR

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Frontiers in Synaptic Neuroscience

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