Kimura Y, Yamada Y, Okada Y
Department of Physiology, School of Medicine, Kobe University, Japan.
Neurosci Lett. 1993 Mar 5;151(1):9-12. doi: 10.1016/0304-3940(93)90032-g.
The postsynaptic field potential (population spike; PS) was recorded from the granule cell layer of guinea pig hippocampal slices after electrical stimulation of the perforant path. Propentofylline, a xanthine derivative, enhanced the amplitude of PS to 120-150% of the original level at a concentration range of 100 nM to 1 mM. Theophylline at concentrations over 10 microM increased the PS amplitude to 200% of the original amplitude. Simultaneous application of 1-(5-isoquin-olinesulfonyl)-2-methylpiperazine dihydrochloride (H-7; 100 microM), a protein kinase C (PKC) inhibitor, significantly blocked the excitatory effect of propentofylline, but it failed to counteract the excitatory effect of theophylline. These results indicate that the excitatory effect of propentofylline is mediated by a metabolic process involving PKC and that the protective effect of propentofylline on neuronal damage caused by hypoxia is not due to the inhibition of synaptic transmission.
在对豚鼠海马切片的穿通通路进行电刺激后，从颗粒细胞层记录突触后场电位（群体峰电位；PS）。黄嘌呤衍生物丙戊茶碱在100 nM至1 mM的浓度范围内可将PS的幅度增强至原始水平的120%至150%。浓度超过10 μM的茶碱可使PS幅度增加至原始幅度的200%。同时应用蛋白激酶C（PKC）抑制剂1-（5-异喹啉磺酰基）-2-甲基哌嗪二盐酸盐（H-7；100 μM）可显著阻断丙戊茶碱的兴奋作用，但无法抵消茶碱的兴奋作用。这些结果表明，丙戊茶碱的兴奋作用是由涉及PKC的代谢过程介导的，并且丙戊茶碱对缺氧引起的神经元损伤的保护作用并非由于抑制突触传递。
