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目的通过对正常和缺氧条件下N-甲基-D-天冬氨酸(NMDA)受体通道特性进行研究,探讨下丘脑神经元缺氧损伤的机理,为临床防治脑缺血/缺氧损伤提供实验依据。方法取材于新生SD大鼠下丘脑视前区/下丘脑前区(PO/AH)神经元,应用膜片钳单通道记录技术对缺氧和非缺氧两种状态下NMDA受体特性进行研究,观察其在缺氧和非缺氧条件下的翻转电位、电流幅度、电导特性的变化。结果神经元缺氧后其通道内向电流幅值由平均(4.501±0.980) pA(n=20,40 mV)上升为(6.000±1.750) pA(n=16,40 mV),优势电导由非缺氧组的(45.693±1.850) pS (n=16)上升为(60.206±1.750) pS(n=10),而翻电位极为接近。结论缺氧是使NMDA受体通道过度激活和Ca2+大量内流的一外因条件。神经元缺氧时,同一钳制电压下其内向电流幅度明显高于对照组,优势电导也有明显上升,可以解释为缺氧引起了神经元Ca2+超载,从而介导了细胞的损伤和死亡。
OBJECTIVE: To investigate the mechanism of hypoxic injury of hypothalamic neurons by studying the characteristics of N-methyl-D-aspartate (NMDA) receptor channels under normal and hypoxic conditions and to provide a basis for clinical prevention and treatment of cerebral ischemia / hypoxia Damage provided experimental basis. METHODS: The hypothalamus preopticus / hypothalamic precancerous (PO / AH) neurons were isolated from neonatal SD rats and the characteristics of NMDA receptors under both hypoxia and non-hypoxia conditions were studied using patch-clamp single channel recording , Observe its changes in reversal potential, current amplitude, conductance characteristics under hypoxic and non-hypoxic conditions. RESULTS: After hypoxia, the inward current amplitude of neurons increased from (4.501 ± 0.980) pA (n = 20,40 mV) to (6.000 ± 1.750) pA (n = 16,40 mV) Oxygen group (45.693 ± 1.850) pS (n = 16) increased to (60.206 ± 1.750) pS (n = 10), while the turn-on potential was very close. Conclusion Hypoxia is an extrinsic condition that causes NMDA receptor channel activation and Ca2 + influx. Neuronal hypoxia, the same clamp voltage inward current amplitude was significantly higher than the control group, the dominant conductance also increased significantly, can be interpreted as hypoxia caused neuronal Ca2 + overload, which mediated cell damage and death.