About this Research Topic
Oligodendrocytes are responsible for myelin formation in the CNS, facilitating fast signal transmission and providing metabolic support. These cells differentiate from oligodendrocyte progenitor cells (OPCs) in the developing and adult CNS, representing about 5–8% of total glial cells.
When a lesion occurs in the adult brain, OPCs migrate and differentiate to remyelinate damaged axons. This process fails when there is chronicization of the disease, and myelin damage becomes permanent.
OPCs are crucial players in neuro-glial communication as they receive synaptic inputs from neurons and express ion channels and neurotransmitter/neuromodulator receptors that control their maturation.
Ion channels are recognized as attractive therapeutic targets. Indeed, ligand-gated and voltage-gated channels can be found among the top five pharmaceutical target groups of FDA-approved agents. The blockage of specific ion channels, such as potassium (i.e., Dalfampridine), sodium (i.e., Phenytoin), and/or calcium (i.e., Pregabalin) channels, ameliorates some of the symptoms of MS and improves the outcome in clinically tested animal models. However, there is still a lack of knowledge as to the specific underlying mechanism regulating the action of ion-channel targeting compounds. This is often due to the wide expression of these channels on neurons, glia, and infiltrating immune cells, making it difficult to exactly describe the underlying regulatory mechanisms.
The aim of this Research Topic is to provide an update and discuss the novel findings on the intricate role of ion channels and metabotropic receptors underlying axonal myelination in health and disease. We aim to combine different and complementary approaches to paint a mechanistic and cell biological view of the role of ion channels and metabotropic receptors in the myelination process by using in vivo, in vitro, and modeling approaches.
We welcome submissions of Original Research, Reviews, Mini-Review, Hypothesis and Theories, Perspective, Clinical Trials, Case Reports, and Opinion articles focusing on, but not limited to the following questions:
· Novel techniques to study the myelination process in vitro and in vivo
· New drugs/chemical compounds to treat demyelinating pathologies
· Contribution of Ion channels and metabotropic receptors on myelination (ex. Potassium currents and glutamate receptors)
· Roles of neuronal and non-neuronal cells in axonal myelination (ex. Oligodendrocytes)
· Interactions between non-neuronal cells in the formation and maintenance of myelin.
· Myelin abnormalities in neurodevelopmental disorders and neurodegenerative diseases.
· Axon-glia protein interactions during development and neurodegenerative diseases.
When a lesion occurs in the adult brain, OPCs migrate and differentiate to remyelinate damaged axons. This process fails when there is chronicization of the disease, and myelin damage becomes permanent.
OPCs are crucial players in neuro-glial communication as they receive synaptic inputs from neurons and express ion channels and neurotransmitter/neuromodulator receptors that control their maturation.
Ion channels are recognized as attractive therapeutic targets. Indeed, ligand-gated and voltage-gated channels can be found among the top five pharmaceutical target groups of FDA-approved agents. The blockage of specific ion channels, such as potassium (i.e., Dalfampridine), sodium (i.e., Phenytoin), and/or calcium (i.e., Pregabalin) channels, ameliorates some of the symptoms of MS and improves the outcome in clinically tested animal models. However, there is still a lack of knowledge as to the specific underlying mechanism regulating the action of ion-channel targeting compounds. This is often due to the wide expression of these channels on neurons, glia, and infiltrating immune cells, making it difficult to exactly describe the underlying regulatory mechanisms.
The aim of this Research Topic is to provide an update and discuss the novel findings on the intricate role of ion channels and metabotropic receptors underlying axonal myelination in health and disease. We aim to combine different and complementary approaches to paint a mechanistic and cell biological view of the role of ion channels and metabotropic receptors in the myelination process by using in vivo, in vitro, and modeling approaches.
We welcome submissions of Original Research, Reviews, Mini-Review, Hypothesis and Theories, Perspective, Clinical Trials, Case Reports, and Opinion articles focusing on, but not limited to the following questions:
· Novel techniques to study the myelination process in vitro and in vivo
· New drugs/chemical compounds to treat demyelinating pathologies
· Contribution of Ion channels and metabotropic receptors on myelination (ex. Potassium currents and glutamate receptors)
· Roles of neuronal and non-neuronal cells in axonal myelination (ex. Oligodendrocytes)
· Interactions between non-neuronal cells in the formation and maintenance of myelin.
· Myelin abnormalities in neurodevelopmental disorders and neurodegenerative diseases.
· Axon-glia protein interactions during development and neurodegenerative diseases.
Keywords: myelin, oligodendrocytes, OPC, axonal myelination, ion channels, Novel biomarkers
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.
