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

为了评价单碳酸转运体对中枢神经系统可兴奋传递的葡萄糖敏感性的作用，我们在第一年使用光敏染料进行了光学技术。低葡萄糖（2 mM）人工脑液浸泡对正常大鼠新鲜脑片隔核或海马10分钟内电刺激传递抑制（60%）。预施用低糖溶液降低了同期低糖溶液对传播的抑制（20%）（急性低血糖适应）。这种适应性在含单碳酸转运蛋白抑制剂的溶液中表现出来。当低糖溶液与正常溶液交换时，含有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。皮下注射nph -胰岛素7 d对慢性低血糖大鼠神经兴奋性的抑制作用比正常大鼠小（30%）（慢性低血糖适应）。在含有MCT抑制剂的溶液中，这种适应在慢性低血糖大鼠的切片中部分减弱。这些数据提示MCT可能调节慢性低血糖大鼠神经元兴奋性抑制的恢复和对低血糖的敏感性。第二年，通过Northern blot分析，我们测量了MCT1-， MCT2-RNA的表达量。在正常大鼠脑中，MCT1-和MCT2-RNA不表达。MCT1-和MCT2-RNA在慢性低血糖大鼠脑中表达量相同。在经低糖溶液预处理的正常大鼠脑中，MCT1-和MCT2-RNA均有轻微表达。采用抗MCT1-和抗mct2抗体的Western blot分析正常大鼠和慢性低血糖大鼠脑内MCT1-和mct2蛋白的表达情况。正常大鼠脑中MCT1-和mct2蛋白均未表达。在慢性低血糖大鼠脑中，MCT1-和mct2蛋白均有相同程度的高表达。这些数据表明，MCT的表达可能在低血糖暴露下增加，MCT功能的增加可能调节神经元兴奋性对低血糖状态的适应。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