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  • Title: Characteristics of the hypoosmosis-induced calcium response in isolated nerve terminals of rat brain.
    Author: Levko AV, Rakovich AA, Samoilenko SG, Konev SV.
    Journal: Med Sci Monit; 2003 Apr; 9(4):BR115-24. PubMed ID: 12709662.
    Abstract:
    BACKGROUND: Cerebral edema contributes significantly to morbidity and death in many common neurological disorders. Ca2+ ions play a important role in the development of pathophysiological reactions in nerve cells. The aim of our research was to elucidate the mechanism of the osmotically-induced entrance of Ca2+ into nerve terminals (synaptosomes) and to estimate the involvement of endoplasmic reticulum Ca2+ stores in intrasynaptosomal Ca2+-dependent processes in hypoosmotic swelling. MATERIAL/METHODS: Synaptosomes were isolated from rat brains. The rates of Ca2+ uptake were determined using 45Ca2+ as a radiotracer. Intracellular Ca2+ measurements were performed using Fura-2 as a cell calcium indicator. RESULTS: Entry into synaptosomes in hypotonic medium (230 mOsm) of osmosis-induced Ca2+ (45 Ca2+) was reduced by verapamil, Cd2+ or genistein to 50-60% of baseline. NEM and PCMB inhibit 45Ca2+ uptake. Swelling of synaptosomes is coupled with increased tyrosine kinase activity and oxidation of SH-groups of cysteine residues of the membrane proteins involved in Ca2+ transport. These membrane processes probably influence the properties of voltage-dependent L-type Ca2+ channels, which increase their conductivity to Ca2+. Activation of RyR- and Ins(1,4,5,)P3-stores were recorded. It was shown that the Ins(1,4,5,)P3-stores are a major source of the increase in [Ca2+]i in the cytoplasm with swelling of the synaptosomes. CONCLUSIONS: Osmotic swelling of synaptosomes leads to Ca2+ accumulation by intrasynaptosomal mitochondria. Excess Ca2+ ions stored in mitochondria inhibit oxidative phosphorylation. This causes an irreversible reduction in the energy status of nerve terminals, which can initiate pathophysiological processes in nerve cells.
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