Fowler J C
Life Sciences Division, Los Alamos National Laboratory, NM 87545.
Brain Res. 1989 Jun 26;490(2):378-84. doi: 10.1016/0006-8993(89)90258-8.
Submerged rat hippocampal slices were exposed to hypoxic medium prepared with 95% N2/5% CO2. The population spikes recorded from CA1 cell layer were completely blocked within a range of 5-10 min. The adenosine antagonist theophylline (100 microM) delayed and partially prevented the hypoxia-induced depression. Increasing concentrations of the more potent adenosine antagonist 8-phenyltheophylline (8-PT; 0.1, 1, 10 microM) resulted in progressively less hypoxia-induced depression. The antidromically elicited afterpotentials recorded in the absence of synaptic transmission in low calcium, high magnesium medium were blocked within 8 min of hypoxia. Theophylline (100 microM) and 8-PT (10 microM) delayed to a similar extent the hypoxia-induced depression of the first afterpotential but did not prevent its complete depression.
将大鼠海马脑片置于用95% N₂/5% CO₂配制的缺氧培养基中。在5 - 10分钟内,从CA1细胞层记录到的群体峰电位完全被阻断。腺苷拮抗剂茶碱(100微摩尔)可延迟并部分防止缺氧诱导的抑制。更有效的腺苷拮抗剂8 - 苯基茶碱(8 - PT;0.1、1、10微摩尔)浓度增加,缺氧诱导的抑制作用逐渐减弱。在低钙、高镁培养基中无突触传递时记录的逆向引发后电位,在缺氧8分钟内被阻断。茶碱(100微摩尔)和8 - PT(10微摩尔)在相似程度上延迟了缺氧诱导的第一个后电位的抑制,但并未阻止其完全抑制。