Intracellular increases in free Calcium (Ca2+) concentration control a variety of essential signaling pathways and cellular processes in neurons and other excitable cell types. Calcium-dependent signaling pathways are switched on by extracellular Ca2+ influx into the cell in co-ordination with Ca2+ release from intracellular stores and are switched off by the concerted action of diverse Ca2+ transporters that remove Ca2+ from the cytoplasm.
This Research Topic will address both fundamental mechanisms that initiate Ca2+ signals, which are not entirely understood, and novel players that shape the Ca2+ responses that initiate activity-mediated functional and structural changes in neurons. Also, this Topic will address how Ca2+ promotes signaling pathways that favor learning and long-term memory or memory loss. In particular, in this Topic we propose to include research articles that address novel Ca2+ signaling mechanisms, which involve the remarkable capacity of neurons to undergo significant changes in response to activation and how this remarkable plasticity is impaired in aging or in pathological conditions that could culminate in neuroinflammation.
To this aim, colleagues are welcomed to contribute with Original Research, Hypothesis and Theory, Review, Mini-Review, and Opinion articles covering, but not limited, to the following topics:
1. Novel molecular interactions and players engaged in Ca2+ regulation/ homeostasis.
2. Compartmentalized Ca2+ signalling and handling in neurons.
3. Novel in vivo and in vitro models to study Ca2+-dependent mechanisms underlying learning and memory.
4. Mechanisms that underlie the generation of activity induced nuclear Ca2+ signals in health and in neurodegenerative diseases.
5. Crosstalk of Ca2+ and ROS between ER and mitochondria in health and disease.
6. Transcriptional mechanisms mediated by Ca2+ in learning and memory.
7. Mechanisms that modulate Ca2+-dependent pathways involved in synaptic plasticity.
8. Novel techniques to measure Ca2+ transients in neuronal circuits with higher temporal and spatial resolution in vivo.
9. Mechanisms of neuroinflammation linked to imbalanced Ca2+ signals and its consequence for neuronal function or survival.
10. Ca2+, ROS, and impairments in ER and Mitochondria during aging.
Intracellular increases in free Calcium (Ca2+) concentration control a variety of essential signaling pathways and cellular processes in neurons and other excitable cell types. Calcium-dependent signaling pathways are switched on by extracellular Ca2+ influx into the cell in co-ordination with Ca2+ release from intracellular stores and are switched off by the concerted action of diverse Ca2+ transporters that remove Ca2+ from the cytoplasm.
This Research Topic will address both fundamental mechanisms that initiate Ca2+ signals, which are not entirely understood, and novel players that shape the Ca2+ responses that initiate activity-mediated functional and structural changes in neurons. Also, this Topic will address how Ca2+ promotes signaling pathways that favor learning and long-term memory or memory loss. In particular, in this Topic we propose to include research articles that address novel Ca2+ signaling mechanisms, which involve the remarkable capacity of neurons to undergo significant changes in response to activation and how this remarkable plasticity is impaired in aging or in pathological conditions that could culminate in neuroinflammation.
To this aim, colleagues are welcomed to contribute with Original Research, Hypothesis and Theory, Review, Mini-Review, and Opinion articles covering, but not limited, to the following topics:
1. Novel molecular interactions and players engaged in Ca2+ regulation/ homeostasis.
2. Compartmentalized Ca2+ signalling and handling in neurons.
3. Novel in vivo and in vitro models to study Ca2+-dependent mechanisms underlying learning and memory.
4. Mechanisms that underlie the generation of activity induced nuclear Ca2+ signals in health and in neurodegenerative diseases.
5. Crosstalk of Ca2+ and ROS between ER and mitochondria in health and disease.
6. Transcriptional mechanisms mediated by Ca2+ in learning and memory.
7. Mechanisms that modulate Ca2+-dependent pathways involved in synaptic plasticity.
8. Novel techniques to measure Ca2+ transients in neuronal circuits with higher temporal and spatial resolution in vivo.
9. Mechanisms of neuroinflammation linked to imbalanced Ca2+ signals and its consequence for neuronal function or survival.
10. Ca2+, ROS, and impairments in ER and Mitochondria during aging.
