The functional role of glucose on the excitability and neurotransmission in neurons of rat septal nucleus

在离体大鼠脑片上，对隔背外侧核（DLSN）和视交叉上核（SCN）神经元进行了细胞内和全细胞膜片钳记录。降低细胞外葡萄糖产生的浓度依赖性超极化与自发放电的动作电位的停止。低血糖引起的超极化与输入膜电阻降低有关，在接近K^+平衡电位时，其极性发生逆转。低氧还引起兴奋性和抑制性突触后电位的抑制。取代2-脱氧-D-葡萄糖，抗代谢葡萄糖底物，模仿这些影响的葡萄糖消耗。甘露庚酮糖（10-20 mM）和二硝基苯酚（50 μ M），有效的氧化磷酸化抑制剂，即使在11 mM葡萄糖的存在下，也产生膜超极化和突触后电位的抑制。磺脲类药物，格列本脲（100 μ M）和甲苯磺丁脲（1 mM），部分降低超极化。采用“切片-贴片”技术在DLSN神经元上记录到低血糖外向电流。膜片破裂后，静息膜电位和输入电阻为-62（）SY ±-。（）4 mV（n=18）和200-300 mOMEGA。经膜片钳注射ATP可抑制低血糖诱发的外向电流，提示低血糖可能通过激活ATP依赖性K^+通道（K^+_ channels）而引起外向电流<ATP>。将葡萄糖降低至低于2 mM可抑制刺激海马伞/穹窿通路引起的兴奋性突触后电流（EPSC）。抑制性突触后电流（IPSC）和晚期超极化电流（LHC）也减少细胞外葡萄糖。葡萄糖耗竭抑制GABA诱导的外向电流，而不抑制谷氨酸诱导的内向电流。这些结果表明，葡萄糖调节神经尿传递

Intracellular and whole-cell patch-clamp recordings were made from neurons in dorsolateral septal nucleus (DLSN) and suprachiasmatic nucleus (SCN) of rat brain slice, in vitro. Lowering extracellular glucose produced a concentration-dependent hyperpolarization associated with a cessation of the spontaneous firing of action potentials. The hypoglycemia-induced hyperpolarization was associated with decreased input membrane resistance and it reversed in polarity at potential near the K^+ equilibrium potential. Hypoglycemia also caused the depression of excitatory and inhibitory postsynaptic potentials. Substitution of 2-Deoxy-D-glucose, an antimetabolic glucose substrate, mimicked these effects of glucose-depletion. Mannoheptulose (10-20 mM) and dinitrophenol (50 muM), potent inhibitors for oxidative phosphorylation, produced both the membrane hyperpolarization and the inhibition of postsynaptic potentials even in the presence of 11 mM glucose. Sulphonylureas, glibenclamide (100 muM) and tolbutamide (1 mM), partially reduced the hyperpolarization. The hypoglycemic outward current was recorded from DLSN neurons by 'slice-patch' technique. After rupturing patch membrane, resting membrane potential and input resistance were -62 (〕SY.+-.〔) 4 mV (n=18) and 200-300 mOMEGA, respectively. Injection of ATP through patch-pipette inhibited the hypoglycemia-induced outward current, suggesting that the hypoglycemia causes the outward current by activation of ATP-dependent K^+ channels (K^+_<ATP> channels). Deprivation of glucose to less than 2 mM depressed excitatory postsynaptic current (EPSC) evoked by stimulations of fimbria/fornix pathway. Inhibitory postsynaptic current (IPSC) and late hyperpolarizing current (LHC) were also reduced by decreasing extracellular glucose. Glucose-depletion depressed GABA-induced outward currents, while it did not depress glutamate-induced inward currents. These results suggest that glucose regulates neurourotransmission