This Research Topic is the second volume of Research Topic "Regulation of AMPA Receptors, from the genetic to the functional level". Please see the first volume
here.
The brain's ability to store and process memory for learning and cognition is determined by synaptic plasticity. This process is defined as the ability of synapses to adapt to 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 AMPA 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 AMPA receptors to synapses. In this sense, the dysfunction of AMPA receptor plasticity is directly linked to symptoms and treatments of neurological and psychiatric disorders.
For instance, AMPA receptor dysfunction underlies various forms of neurodegenerative diseases. Aging, the main risk factor for neurodegeneration, has been associated with the dysregulation of AMPA receptors. The antidepressant effects of ketamine could be related to plastic changes in AMPAR. Molecular changes in AMPA receptor are associated with neurodevelopmental and rare brain disorders. Finally, neuroinflammation processes, which have been implicated in various psychiatric disorders, are related to changes in AMPA receptor functions.
Therefore, it is timely to understand the mechanisms involved in the regulation of AMPA receptors in brain diseases, and welcome submissions that address the following points:
1. Regulation of the expression and trafficking of AMPARs
2. Genetic and epigenetic remodeling of AMPAR plasticity
3. Novel techniques and new insights into examining the plasticity of AMPAR
4. New findings into the Role of AMPAR plasticity in neurological and psychiatric disorders
5. New findings into the Role of glia on the expression and function of AMPAR
This Research Topic is the second volume of Research Topic "Regulation of AMPA Receptors, from the genetic to the functional level". Please see the first volume
here.
The brain's ability to store and process memory for learning and cognition is determined by synaptic plasticity. This process is defined as the ability of synapses to adapt to 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 AMPA 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 AMPA receptors to synapses. In this sense, the dysfunction of AMPA receptor plasticity is directly linked to symptoms and treatments of neurological and psychiatric disorders.
For instance, AMPA receptor dysfunction underlies various forms of neurodegenerative diseases. Aging, the main risk factor for neurodegeneration, has been associated with the dysregulation of AMPA receptors. The antidepressant effects of ketamine could be related to plastic changes in AMPAR. Molecular changes in AMPA receptor are associated with neurodevelopmental and rare brain disorders. Finally, neuroinflammation processes, which have been implicated in various psychiatric disorders, are related to changes in AMPA receptor functions.
Therefore, it is timely to understand the mechanisms involved in the regulation of AMPA receptors in brain diseases, and welcome submissions that address the following points:
1. Regulation of the expression and trafficking of AMPARs
2. Genetic and epigenetic remodeling of AMPAR plasticity
3. Novel techniques and new insights into examining the plasticity of AMPAR
4. New findings into the Role of AMPAR plasticity in neurological and psychiatric disorders
5. New findings into the Role of glia on the expression and function of AMPAR