Experimental diabetes enhances Ca2+ mobilization and glutamate exocytosis in cerebral synaptosomes from mice - PubMed (original) (raw)

Experimental diabetes enhances Ca2+ mobilization and glutamate exocytosis in cerebral synaptosomes from mice

Eiki Satoh et al. Diabetes Res Clin Pract. 2008 Aug.

Abstract

The present study was conducted to investigate the effects of the diabetic condition on the Ca(2+) mobilization and glutamate release in cerebral nerve terminals (synaptosomes). Diabetes was induced in male mice by intraperitoneal injection of streptozotocin. Cytosolic free Ca(2+) concentration ([Ca(2+)](i)) and glutamate release in synaptosomes were determined using fura-2 and enzyme-linked fluorometric assay, respectively. Diabetes significantly enhanced the ability of the depolarizing agents K(+) and 4-aminopyridine (4-AP) to increase [Ca(2+)](i). In addition, diabetes significantly enhanced K(+)- and 4-AP-evoked Ca(2+)-dependent glutamate release. The pretreatment of synaptosomes with a combination of omega-agatoxin IVA (a P-type Ca(2+) channel blocker) and omega-conotoxin GVIA (an N-type Ca(2+) channel blocker) inhibited K(+)- or 4-AP-induced increases in [Ca(2+)](i) and Ca(2+)-dependent glutamate release in synaptosomes from the control and diabetic mice to a similar extent, respectively. These results indicate that diabetes enhances a K(+)- or 4-AP-evoked Ca(2+)-dependent glutamate release by increasing [Ca(2+)](i) via stimulation of Ca(2+) entry through both P- and N-type Ca(2+) channels.

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