About this Research Topic
α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors are the main excitatory neurotransmitter receptors in the brain. AMPA receptors are known to form tetrameric assemblies consisting of GluA1-4 subunits. It has been found that GluA2 subunit-lacking AMPA receptors are permeable to Ca2+ ions (calcium permeable AMPA, CP-AMPA). Being found to be a driving force for plastic changes at synapses of interneurons at different brain regions CP-AMPA receptors attract attention as parallel way to NMDA receptors-mediated induction of synaptic plasticity. Further it was found that regulation of GluA subunits composition, trafficking and regulation of CP-AMPA receptor activity and Ca2+ permeability via phosphorylation/dephosphorylation are important determinants of synaptic plasticity. For example, activity dependent relieve from polyamine block of CP-AMPA receptors at postsynaptic membrane underlies short-term synaptic plasticity; recruiting of CP-AMPA receptors at excitatory synapses upon theta burst stimulation can cause long-term plasticity; and synaptic scaling of CP-AMPA receptors is one of the mechanisms showed for homeostatic plasticity. Thus, being involved in the regulation of synaptic plasticity at different time scales, CP-AMPA receptors provide a foundation for normal brain function and are of high interest as targets for therapeutic interventions against neurodegenerative and psychiatric disorders.
Further investigation of fine mechanisms regulating CP-AMPA function and CP-AMPA-mediated regulation of synaptic plasticity at physiological conditions as well as studies of impaired synaptic plasticity associated with dysregulation/dysfunction of CP-AMPA are of high relevance. We invite interested authors to contribute to the Research Topic submitting their studies that further shed the light on the involvement of CP-AMPA in the regulation of synaptic plasticity in the nervous system. Studies utilizing state-of-art techniques as a combination of whole-cell patch clamp with multiphoton microscopy, Ca2+-imaging, uncaging, optogenetic will be especially encouraged to apply. But authors studying the subject by means of other conventional techniques including methods of molecular biology and biochemistry, pharmacological and behavioral approaches are also encouraged to submit their findings.
We encourage investigators to contribute to the following subjects of the Research Topic:
1. GPCR and TRK receptors-mediated regulation of CP-AMPA function via different signaling pathways and its implication to synaptic plasticity in nervous system.
2. Regulation of transient expression and turnover of CP-AMPA and its role in the induction of synaptic plasticity upon different paradigms (short-, long-term synaptic and homeostatic plasticity) at synapses of primary neurons and interneurons of different brain regions.
3. Role CP-AMPA receptors in synaptic plasticity impairment associated with neuroinflammation, neurodegenerative and psychiatric disorders.
Both review and research papers will be considered for publication. In particular we would like to invite authors to submit for:
1. Short mini reviews highlighting recent findings in CP-AMPA-mediated regulation of synaptic plasticity with critical assessment and conceptualization of obtained results.
2. Retrospective reviews discussing discoveries on the role CP-AMPA in the regulation of synaptic plasticity at different brain regions,
3. Full-length papers and short communications reporting new findings on the aforementioned topics, and
4. Full-length papers and short communications reporting negative results on the role of CP-AMPA in the regulation of synaptic plasticity at certain conditions and brain regions.
Further investigation of fine mechanisms regulating CP-AMPA function and CP-AMPA-mediated regulation of synaptic plasticity at physiological conditions as well as studies of impaired synaptic plasticity associated with dysregulation/dysfunction of CP-AMPA are of high relevance. We invite interested authors to contribute to the Research Topic submitting their studies that further shed the light on the involvement of CP-AMPA in the regulation of synaptic plasticity in the nervous system. Studies utilizing state-of-art techniques as a combination of whole-cell patch clamp with multiphoton microscopy, Ca2+-imaging, uncaging, optogenetic will be especially encouraged to apply. But authors studying the subject by means of other conventional techniques including methods of molecular biology and biochemistry, pharmacological and behavioral approaches are also encouraged to submit their findings.
We encourage investigators to contribute to the following subjects of the Research Topic:
1. GPCR and TRK receptors-mediated regulation of CP-AMPA function via different signaling pathways and its implication to synaptic plasticity in nervous system.
2. Regulation of transient expression and turnover of CP-AMPA and its role in the induction of synaptic plasticity upon different paradigms (short-, long-term synaptic and homeostatic plasticity) at synapses of primary neurons and interneurons of different brain regions.
3. Role CP-AMPA receptors in synaptic plasticity impairment associated with neuroinflammation, neurodegenerative and psychiatric disorders.
Both review and research papers will be considered for publication. In particular we would like to invite authors to submit for:
1. Short mini reviews highlighting recent findings in CP-AMPA-mediated regulation of synaptic plasticity with critical assessment and conceptualization of obtained results.
2. Retrospective reviews discussing discoveries on the role CP-AMPA in the regulation of synaptic plasticity at different brain regions,
3. Full-length papers and short communications reporting new findings on the aforementioned topics, and
4. Full-length papers and short communications reporting negative results on the role of CP-AMPA in the regulation of synaptic plasticity at certain conditions and brain regions.
Keywords: calcium permeable AMPA, CP-AMPA, GluA2-lacking AMPA, GluA1, GluA3, GluA4, synapse, short-term plasticity, long term plasticity, homeostatic plasticity, neurons, interneurons, trafficking, expression, post translational modification, phosphorylation, dephosphorylation, GPCR, TRK, neurodegeneration, neuroinflamation, psychiatric disorders
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
