Ben-Ari Y, Cherubini E
INSERM U-29, Hôpital de Port-Royal, Paris, France.
Neurosci Lett. 1988 Aug 1;90(3):273-8. doi: 10.1016/0304-3940(88)90201-7.
The effects of brief anoxic episodes on rat CA3 hippocampal neurons were studied with intracellular and extracellular techniques in the in vitro slice preparation. After repeated (3-7 times), brief (2-6 min duration each) applications of artificial cerebrospinal fluid (ACSF) saturated with 95% N2 and 5% CO2, electrical stimulation of various inputs to CA3 neurons, evoked an excitatory postsynaptic potential (EPSP) followed by an all-or-none burst. This response which persisted for several hours after the last anoxic episode, is reminiscent of the bursts induced by various convulsive agents. Post anoxic bursts are generated by a polysynaptic network which converge on the apical distal segment of CA3 neurons. It is concluded that a repetitive impairement of metabolism produces long lasting changes in the synaptic properties of CA3 neurons.
采用细胞内和细胞外技术，在体外脑片标本中研究了短暂缺氧发作对大鼠海马CA3区神经元的影响。在重复（3 - 7次）应用含95% N2和5% CO2饱和的人工脑脊液（ACSF），每次持续短暂时间（2 - 6分钟）后，对CA3神经元的各种输入进行电刺激，诱发兴奋性突触后电位（EPSP），随后出现全或无爆发。这种反应在最后一次缺氧发作后持续数小时，类似于各种惊厥剂诱发的爆发。缺氧后爆发由汇聚在CA3神经元顶端远端节段的多突触网络产生。结论是，代谢的反复受损会导致CA3神经元突触特性发生长期变化。
