About this Research Topic
Calcium (Ca2+) controls a variety of fundamental and universal cellular processes and signaling pathways in neurons and other excitable cell types. Calcium-dependent cellular and molecular processes are switched on by extracellular Ca2+ influx into the cell or by 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 not be limited to address fundamental mechanisms that initiate Ca2+ signals, which are not completely decoded, but will also position novel players that shape the Ca2+ responses that initiate activity-mediated functional and structural changes in synapses. Also, we will address how some important Ca2+ responses may favor learning and memory processes. In particular, we propose to tackle novel mechanisms, which involve the striking neuronal capacity to undergo significant changes in response to activation, and how this remarkable plasticity of neuronal cells is impaired in pathological conditions. 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 features participating in Ca2+ homeostasis
2. Compartmentalized Ca2+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 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 calcium transients during behavioral tasks that allow improvement in the exploration of neuronal circuits with higher temporal and spatial resolution
Keywords: Ca+2 homeostasis, Ca+2 signaling, synaptic plasticity, oxidative agents, mechanisms of learning and memory, synaptopathy
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