About this Research Topic
Transition metals such as zinc, copper, and iron are integrated in various neuronal processes. Zinc, in particular, exhibits a narrow window between benefit and harm, serving as a modulator of synaptic transmission (at low concentrations) or inducing neurotoxicity when it is highly abundant, which impacts the central nervous system. Zinc-induced neurotoxicity is primarily triggered by ion influx through L-type and N-type voltage-dependent calcium channels (VDCCs) and NMDA receptors, as well as zinc release from intracellular stores, leading to cellular dysfunction and eventual cell death. Additionally, copper and iron contribute to neuronal dysfunctions and are commonly associated with neurodegenerative diseases such as Parkinson's and Alzheimer's.
Concurrently, the exposure to transition metals is assumed to drive neuroinflammation dependent on oxidative stress. The reactive oxygen species (ROS), which are mainly generated in mitochondria, are implicated in neuronal apoptotic and necrotic mechanisms due to the oxidation of proteins, phospholipids, and nucleic acids by radicals like superoxide (O2.) and hydroxyl (. OH). The correlation between cytosolic zinc elevation, oxidative stress, and neurotoxicity suggests a direct association between zinc influx and ROS formation. Similar investigations could be extended to other transition metals.
Therefore, we seek to delineate the impact of transition metals on neurotoxicity induced by hypobaric hypoxia and/or ischemia. This research endeavor may encompass electrophysiological studies (intracellular or extracellular recordings), imaging techniques, quantitative fluorescence measurements, and more.
We invite original research articles, reviews, mini-reviews, brief research reports, and perspectives covering various topics, including but not limited to:
• Zinc signaling, entry pathways, and homeostasis.
• ROS signaling.
• Hypoxia and its neurological consequences.
• Ischemia.
• Mitochondria bioenergetics and the role of the respiratory chain.
• Transition metal transporters (e.g. ZIP, ZnTs).
• Impact of hypoxia and ROS on synaptic plasticity, including long-term potentiation (LTP), long term depression and brain circuits.
• Influence of wastewater and wastewater treatments on neurotoxicity.
Concurrently, the exposure to transition metals is assumed to drive neuroinflammation dependent on oxidative stress. The reactive oxygen species (ROS), which are mainly generated in mitochondria, are implicated in neuronal apoptotic and necrotic mechanisms due to the oxidation of proteins, phospholipids, and nucleic acids by radicals like superoxide (O2.) and hydroxyl (. OH). The correlation between cytosolic zinc elevation, oxidative stress, and neurotoxicity suggests a direct association between zinc influx and ROS formation. Similar investigations could be extended to other transition metals.
Therefore, we seek to delineate the impact of transition metals on neurotoxicity induced by hypobaric hypoxia and/or ischemia. This research endeavor may encompass electrophysiological studies (intracellular or extracellular recordings), imaging techniques, quantitative fluorescence measurements, and more.
We invite original research articles, reviews, mini-reviews, brief research reports, and perspectives covering various topics, including but not limited to:
• Zinc signaling, entry pathways, and homeostasis.
• ROS signaling.
• Hypoxia and its neurological consequences.
• Ischemia.
• Mitochondria bioenergetics and the role of the respiratory chain.
• Transition metal transporters (e.g. ZIP, ZnTs).
• Impact of hypoxia and ROS on synaptic plasticity, including long-term potentiation (LTP), long term depression and brain circuits.
• Influence of wastewater and wastewater treatments on neurotoxicity.
Keywords: Hippocampus, fluorescence, cell death, mitochondria, neurodegeneration, transition metals, neurotoxicity, ROS
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