摘要： 目的·探讨ATP敏感钾通道（ATP-sensitive potassium channel，K
ATP）在突触可塑性实验模型长时程增强（long-term potentiation，LTP）的诱导和维持阶段的不同作用。方法·采用5~6周龄雄性C57BL/6小鼠，制备急性脑海马切片。在海马谢弗侧枝CA3-CA1投射通路以场电位的电生理记录方式检测K
ATP的开放激活对基础水平突触传递的影响；通过高频刺激诱导LTP并分别检测在诱导和维持阶段开放K
ATP对突触传递强度的影响；采用氧糖剥夺模型抑制脑片代谢水平以病理性激活K
ATP，并检测K
ATP阻断剂甲苯磺丁脲（tolbutamide，TOL）预处理对氧糖剥夺模型造成的海马LTP损伤的预防作用。结果·K
ATP的开放状态不影响基础水平的突触传递，也不影响LTP的诱导过程，但显著降低LTP维持阶段的幅度。TOL预处理可显著改善糖氧剥夺造成的LTP损伤。结论·K
ATP在生理和病理条件下均对海马LTP的维持起负向调节作用。
关键词: ATP敏感钾通道, 长时程增强, 突触可塑性 Abstract: Objective·To investigate the regulatory roles of ATP-sensitive potassium channel (KATP) in the induction and maintenance stages of long-term potentiation (LTP), which is an experimental model for studies of synaptic plasticity and memory.
Methods·Acute brain slices were prepared from male C57BL/6 mice at 5?6 weeks of age. Electrophysiological recording of the field excitatory postsynaptic potentials was performed at the hippocampal Schaffer collateral-commissural pathway. KATP opener cromakalim was used to activate KATP at basal level, induction and maintenance stages of LTP. Oxygen-glucose deprivation (OGD) was used to induce hypoxia and pathological opening of KATP at the maintenance stage of LTP. Tolbutamide (TOL) was used to block KATP before OGD treatment.
Results·KATP opening showed no effects on basal synaptic transmission and the induction of LTP, but largely decreased the magnitude of LTP at maintenance stage. OGD rapidly impaired LTP maintenance, which was significantly prevented by TOL pre-treatment.
Conclusion·KATP negatively regulates hippocampal LTP maintenance in both physiological and pathological conditions.
Key words: ATP-sensitive potassium channel (KATP), long-term potentiation (LTP), synaptic plasticity PDF全文下载地址:
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