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Making time and space for calcium control of neuron activity
Journal article   Open access   Peer reviewed

Making time and space for calcium control of neuron activity

Joanna Jȩdrzejewska-Szmek, Daniel B. Dorman and Kim T. Blackwell
Current opinion in neurobiology, Vol.83, pp.102804-102804
12/01/2023
DOI: 10.1016/j.conb.2023.102804
PMCID: PMC10842147
PMID: 37913687
url
https://pmc.ncbi.nlm.nih.gov/articles/PMC10842147/pdf/nihms-1938131.pdfView
Open Access

Abstract

Calcium directly controls or indirectly regulates numerous functions that are critical for neuronal network activity. Intracellular calcium concentration is tightly regulated by numerous molecular mechanisms because spatial domains and temporal dynamics (not just peak amplitude) are critical for calcium control of synaptic plasticity and ion channel activation, which in turn determine neuron spiking activity. The computational models investigating calcium control are valuable because experiments achieving high spatial and temporal resolution simultaneously are technically unfeasible. Simulations of calcium nanodomains reveal that specific calcium sources can couple to specific calcium targets, providing a mechanism to determine the direction of synaptic plasticity. Cooperativity of calcium domains opposes specificity, suggesting that the dendritic branch might be the preferred computational unit of the neuron. •Calcium dynamics during in vivo conditions are influenced by immobile buffers and vesicle release.•The size of calcium domains change over time; thus, high specificity coupling evolves to lower specificity activation.•Cooperativity of synaptic inputs opposes spatial specificity, which is restored by inhibitory mechanisms.•Calcium release from stores may promote synaptic plasticity by prolonging the calcium signal.
Calcium release Computational model Nanodomains Stochastic Synaptic plasticity

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