About this Research Topic
Ion channel function or dysfunction plays an important role in neurological and neurodegenerative conditions such as chronic pain, motor disorders, epilepsy, Parkinson’s, Huntington’s and Alzheimer’s disease, Amyotrophic lateral sclerosis and schizophrenia. Convergent efforts between neuroscientists to establish a link between clinical neurology, genetics, loss of function of important proteins and channelopathies behind neurological disorders have become an intense area of research interest. Several ion channels, a group of membrane spanning proteins that regulate ion content and membrane potential in cells, have been implicated as important players in these diseases. Such channels are critically important for the normal function of the brain and excitable tissues.
While many Ca2+ conducting channels (CaV, P2X or glutamate receptors) may contribute to glutamate overload and excitotoxicity directly, K+ channels may also regulate the membrane potential controlling Ca2+ signal indirectly. Therefore, neurologic symptoms associated with these diseases may be treated by decreasing intracellular Ca2+ concentrations through the blockade of voltage-gated potassium channels (e.g., Kv1.3, Kv3.4), glutamate receptors (e.g., NMDA), or activation of nicotinic acetylcholine receptors (e.g., nAChRα7), amongst many others.
The overarching goal of this Research Topic is to provide a platform for researchers to globalize their cutting-edge research regarding the role of channelopathies and modulation thereof in the prevention and/or treatment of neurological disorders. The Research Topic will include (but is not limited to) pharmacologically relevant molecular studies on ion channels and compounds targeting various ion channels and molecular mechanisms to prevent and treat neurodegenerative diseases.
We welcome Original Research and Review articles related, but not limited to, the following subtopics:
• Structural dynamics, regulation, and roles in excitability or ion transport of voltage- and ligand-gated ion channels.
• Pharmacological studies on ion channels and the implication thereof in neurodegeneration.
• Molecular mechanisms and modulation of ion channels to prevent and treat neurodegenerative diseases.
• Design and development of novel modulators of ion channels that may find application in neurological disorders.
While many Ca2+ conducting channels (CaV, P2X or glutamate receptors) may contribute to glutamate overload and excitotoxicity directly, K+ channels may also regulate the membrane potential controlling Ca2+ signal indirectly. Therefore, neurologic symptoms associated with these diseases may be treated by decreasing intracellular Ca2+ concentrations through the blockade of voltage-gated potassium channels (e.g., Kv1.3, Kv3.4), glutamate receptors (e.g., NMDA), or activation of nicotinic acetylcholine receptors (e.g., nAChRα7), amongst many others.
The overarching goal of this Research Topic is to provide a platform for researchers to globalize their cutting-edge research regarding the role of channelopathies and modulation thereof in the prevention and/or treatment of neurological disorders. The Research Topic will include (but is not limited to) pharmacologically relevant molecular studies on ion channels and compounds targeting various ion channels and molecular mechanisms to prevent and treat neurodegenerative diseases.
We welcome Original Research and Review articles related, but not limited to, the following subtopics:
• Structural dynamics, regulation, and roles in excitability or ion transport of voltage- and ligand-gated ion channels.
• Pharmacological studies on ion channels and the implication thereof in neurodegeneration.
• Molecular mechanisms and modulation of ion channels to prevent and treat neurodegenerative diseases.
• Design and development of novel modulators of ion channels that may find application in neurological disorders.
Keywords: Ion channels, neurodegeneration, neuroprotection, channelopathies, channel modulators
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.
