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Extracellular calcium depletion in synaptic transmission
Jonathan E Cohen1, R Douglas Fields
1National Institutes of Health, National Institute for Child and Human Development, Section on Nervous System Development and Plasticity, Bethesda, MD 20892, USA.
Summary
Extracellular calcium ([Ca]o(2+)) levels significantly decrease with neuronal activity, impacting brain function. This calcium depletion acts as a messenger regulating nervous system processes like learning and disease.
Area of Science:
- Neuroscience
- Neurophysiology
- Calcium Signaling
Background:
- Extracellular calcium ([Ca]o(2+)) homeostasis is crucial for neuronal function.
- Neuronal activity, including action potentials and synaptic transmission, significantly reduces [Ca]o(2+).
Purpose of the Study:
- To investigate the role of extracellular calcium ([Ca]o(2+)) regulation in neuronal function.
- To understand how activity-dependent changes in [Ca]o(2+) influence intracellular signaling and neuronal excitability.
Main Methods:
- Utilized modeling studies and recent experimental measurements.
- Analyzed the impact of [Ca]o(2+) changes on ion channels, neurotransmitter receptors, and Ca(2+)-sensitive receptors.
Main Results:
- Modest neuronal activity leads to significant reductions in extracellular calcium ([Ca]o(2+)).
- Changes in [Ca]o(2+) modulate intracellular signaling enzymes like Ca2+/calmodulin-dependent protein kinase II.
- Altered [Ca]o(2+) affects neuronal function at both synaptic and nonsynaptic sites.
Conclusions:
- Extracellular calcium ([Ca]o(2+)) depletion serves as an activity-dependent extracellular messenger.
- This mechanism regulates nervous system function during development, learning, and in disease states.