The effect of insulin injections and long-term administration of the calcium channel blocker nimodipin on depolarization-induced calcium signals was studied in neurons isolated from the dorsal root ganglia of mice with streptozotocin-induced diabetes. Induction of diabetes in mice was followed by slowing of the calcium signal decay kinetics in small neurons (mainly related to the transmission of nociceptive signals). Subcutaneous insulin injections (1 U/kg) tended to normalize the parameters of calcium signals modified by diabetes. Preliminary 3-week-long peroral administration of nimodipin (40 mg/kg) increased the peak amplitude of depolarization-induced calcium signals in isolated neurons and caused spontaneous activity usually absent in the cells under control conditions. Kinetics of calcium transients in this case remained slow. It was concluded that hyperglycemia and related impairments of the surplus Ca2+ extrusion mechanisms play an essential role in genesis of the changes in calcium signals caused by streptozotocin-induced diabetes.
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