About this Research Topic
It is with great pleasure that we announce a new Research Topic on “Potassium channels and calcium signaling in physiology and pathophysiology of the brain” in the Frontiers in Pharmacology Journal. This Research Topic will include research articles and review papers on the topic. All submissions will be subjected to a peer-review process, according to the guidelines of Frontiers in Pharmacology.
Potassium channels have an essential regulatory role in neurons and in subcellular organelles, such as mitochondria, for controlling neuronal excitability, calcium signaling and mitochondrial functions. These potassium channel-dependent regulations of calcium influx are important for long-term potentiation processes and formation/function of dendritic spines. They are related to physiological functions of learning and memory and their dysfunction was associated with behavioral impairments towards anxiety and deficits in learning and memory. During aging or in neurodegenerative conditions their expression and function was found drastically altered. Therefore, such dysfunction of potassium channel activity might result in a failure to regulate neuronal excitability and increased Ca2+ concentrations, triggering delayed neuronal death.
Alteration of intracellular calcium levels occurs in several neurodegenerative disorders at different stages during the progression of neuropathology. These calcium deregulations are accompanied by neuronal hypo/hyperexcitability with effects on neuronal vulnerability towards toxic stimuli. Moreover, in neurons, deregulation of intracellular calcium influences multiple metabolic processes, thereby promoting progressive cell death. Although substantial data was accumulated over the recent years, there are still several open questions that remain to be addressed. What is the relationship between calcium homeostasis and potassium channels in physiological and pathological conditions? How does calcium deregulation influence neuronal excitability and neuronal death? What are the major regulators of calcium deregulation and how can they modulate potassium channel activity? Is excitotoxicity a cause or a consequence of potassium channel dysfunction or of calcium deregulation? Through this Research Topic, we encourage experts in the field of potassium channels and calcium signaling to address these and other critical questions. Furthermore, discussions of new concepts and paradigms are highly appreciated.
This Research Topic of Frontiers of Pharmacology on “Potassium channels and calcium signaling in physiology and pathophysiology of the brain” aims to explore how potassium channels influence calcium signaling and neuronal fate, how they operate, their pharmacological modulators and their function in physiological and pathophysiological conditions.
Potassium channels have an essential regulatory role in neurons and in subcellular organelles, such as mitochondria, for controlling neuronal excitability, calcium signaling and mitochondrial functions. These potassium channel-dependent regulations of calcium influx are important for long-term potentiation processes and formation/function of dendritic spines. They are related to physiological functions of learning and memory and their dysfunction was associated with behavioral impairments towards anxiety and deficits in learning and memory. During aging or in neurodegenerative conditions their expression and function was found drastically altered. Therefore, such dysfunction of potassium channel activity might result in a failure to regulate neuronal excitability and increased Ca2+ concentrations, triggering delayed neuronal death.
Alteration of intracellular calcium levels occurs in several neurodegenerative disorders at different stages during the progression of neuropathology. These calcium deregulations are accompanied by neuronal hypo/hyperexcitability with effects on neuronal vulnerability towards toxic stimuli. Moreover, in neurons, deregulation of intracellular calcium influences multiple metabolic processes, thereby promoting progressive cell death. Although substantial data was accumulated over the recent years, there are still several open questions that remain to be addressed. What is the relationship between calcium homeostasis and potassium channels in physiological and pathological conditions? How does calcium deregulation influence neuronal excitability and neuronal death? What are the major regulators of calcium deregulation and how can they modulate potassium channel activity? Is excitotoxicity a cause or a consequence of potassium channel dysfunction or of calcium deregulation? Through this Research Topic, we encourage experts in the field of potassium channels and calcium signaling to address these and other critical questions. Furthermore, discussions of new concepts and paradigms are highly appreciated.
This Research Topic of Frontiers of Pharmacology on “Potassium channels and calcium signaling in physiology and pathophysiology of the brain” aims to explore how potassium channels influence calcium signaling and neuronal fate, how they operate, their pharmacological modulators and their function in physiological and pathophysiological conditions.
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.
