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Synaptosomal [Ca2+]i as influenced by Na+/Ca2+ exchange and K+ depolarization
C B Duarte1, C A Carvalho, I L Ferreira
1Department of Zoology, University of Coimbra, Portugal.
Cell Calcium
|October 1, 1991
Summary
Sodium-calcium exchange regulates intracellular calcium levels in synaptosomes. Elevated calcium via this exchange reduces calcium influx through voltage-dependent channels, impacting neurotransmitter release.
Area of Science:
- Neuroscience
- Cellular Biology
- Biochemistry
Background:
- Intrasynaptosomal calcium concentration ([Ca2+]i) is critical for neuronal function.
- Sodium-calcium (Na+/Ca2+) exchange plays a role in regulating [Ca2+]i.
- Voltage-dependent calcium channels are key mediators of calcium influx into neurons.
Purpose of the Study:
- To investigate how Na+/Ca2+ exchange modulates intrasynaptosomal Ca2+ concentration.
- To determine the interplay between Na+/Ca2+ exchange and voltage-dependent calcium channels in regulating [Ca2+]i.
- To explore the impact of altered sodium gradients on Ca2+ dynamics.
Main Methods:
- Utilized Indo-1 fluorescence to measure intracellular Ca2+ ([Ca2+]i).
- Manipulated extracellular sodium gradients using Li+ or choline substitution.
- Measured 45Ca2+ influx and [Ca2+]i under various conditions, including K+ depolarization.
Main Results:
- Increased [Ca2+]i via Na+/Ca2+ exchange significantly reduced Ca2+ influx through voltage-dependent channels.
- A [Ca2+]i of ~650 nM from Na+/Ca2+ exchange halved K+-induced Ca2+ entry.
- Pre-elevated [Ca2+]i above ~800 nM or predepolarization in Ca-free medium inhibited Ca2+ channel entry by at least 40%.
- Lithium in the external medium reduced synaptosomal buffering capacity, potentially by releasing mitochondrial Ca2+.
Conclusions:
- Na+/Ca2+ exchange acts as a significant regulator of Ca2+ influx via voltage-dependent channels.
- This modulation by Na+/Ca2+ exchange likely influences neurotransmitter release.
- Synaptosomal Ca2+ buffering capacity is affected by external ions like Li+.