Role of Monocarbonic Acid Transporter on the Glucose-Sensitiveness of the Central Nervous System in the Insulin inducing Hypoglycemic Rat

为了评价一碳酸转运体在中枢神经系统兴奋性传递的葡萄糖敏感性中的作用，我们在第一年使用光敏染料进行了光学技术。在正常大鼠的新鲜脑片上，水浴应用低葡萄糖（2 mM）人工脑液在10分钟内诱导电刺激隔核或海马传递的抑制（60%）。预先应用低葡萄糖溶液降低了相同时间段内低葡萄糖溶液对传输的抑制（20%）（对低血糖的急性适应）。这种适应在含一碳酸转运蛋白抑制剂的溶液中显示。当将低葡萄糖溶液更换为正常溶液时，在含MCT抑制剂的溶液中，神经兴奋性抑制的恢复时间延长了1.5倍。慢性低血糖脑片神经兴奋性的抑制 ...更多信息 皮下注射NPH-胰岛素7天的大鼠与正常大鼠的脑片相比（慢性低血糖适应）更小（30%）。在含MCT抑制剂的溶液中，慢性低血糖大鼠切片中的这种适应性部分减弱。这些数据表明，MCT可能调节慢性低血糖大鼠从低血糖引起的神经元兴奋性抑制中恢复以及对低血糖的敏感性。第二年，采用北方印迹分析法检测MCT 1-、MCT 2-RNA的表达量。在正常大鼠脑中，没有MCT 1-和MCT 2-RNA的表达。然而，在慢性低血糖大鼠脑中，MCT 1-和MCT 2-RNA以相同的量表达。在正常大鼠脑组织中，低浓度葡萄糖溶液预处理后，MCT 1-和MCT 2-RNA有少量表达。利用抗MCT 1-和抗MCT 2-抗体进行Western blot分析，检测正常大鼠和慢性低血糖大鼠脑中MCT 1-和MCT 2-蛋白的表达。在正常大鼠脑中，没有MCT 1-和MCT 2-蛋白的表达。在慢性低血糖大鼠脑中，MCT 1-和MCT 2-蛋白以相同程度高表达。这些数据表明，暴露于低血糖可能会增加大脑中MCT的表达，MCT功能的增加可能会调节神经元兴奋性对低血糖条件的适应。少

To evaluate the role of monocarbonic acid transporter on the glucose sensitiveness of excitable transmission in the central nervous system, we performed optical technique by using photo-sensitive dye in the first year. Bath application of low glucose (2 mM) artificial cerebral fluid induced suppression (60%) of the transmission by electrical stimulation within 10 minutes in the septal nucleus or hippocampus of the fresh brain slices of normal rats. Pre-application of low glucose solution decreased the suppression (20%) of the transmission by low glucose solution in the same period of time (Acute adaptation against hypoglycemia). This adaptation was shown in monocarbonic acid transporter inhibitor containing solution. When the low glucose solution was exchanged to the normal solution, recovery time from suppression of neural excitability was prolonged one and half times in the MCT inhibitor containing solution. The suppression of neural excitability in the slices of chronic hypoglycemic … More rats made by 7 days subcutaneous NPH-insulin injection was smaller (30%) in comparison with the slices of normal rats (Chronic adaptation against hypoglycemia). In the MCT inhibitor containing solution, this adaptation was partially attenuated in the slices of the chronic hypoglycemic rats. These data suggest that MCT might modulate the recovery from suppression of neuronal excitability by hypoglycemia and the sensitivity to hypoglycemia in the chronic hypoglycemic rats. In the second year, by using the Northern blot analysis, we measured expression amount of MCT1-, MCT2-RNA. In the normal rat brain, no MCT1- and MCT2-RNA were expressed. However both MCT1- and MCT2-RNA were expressed in the chronic hypoglycemic rat brain at the same amount. In the normal rat brain pretreated with low glucose solution, MCT1- and MCT2-RNA were slightly expressed. By using Western blot analysis with anti-MCT1- and anti-MCT2 antibody, we analyzed the expression of MCT1- and MCT2-protein in the brain of the normal rats and the chronic hypoglycemic rats. In the normal rat brain, no MCT1- and MCT2-protein were expressed. In the chronic hypoglycemic rat brain, both MCT1- and MCT2-protein were highly expressed at the same degree. These data suggest that expression of MCT might be increased in the brain by exposure of hypoglycemia and that increase of MCT function might modulate the adaptation of neuronal excitability against hypoglycemic condition. Less