Cyclosporin ameliorates traumatic brain-injury-induced alterations of hippocampal synaptic plasticity
Cyclosporin ameliorates traumatic brain-injury-induced alterations of hippocampal synaptic plasticity
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DOI：
10.1006/exnr.1999.7338
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发表时间：
2000-04-01
影响因子：
5.3
通讯作者：
Mattson, MP
中科院分区：
文献类型：
--
作者：
Albensi, BC;Sullivan, PG;Mattson, MP
虽然创伤性脑损伤（TBI）经常导致学习和记忆功能受损，但其潜在机制尚不清楚，目前还没有可以保护这些功能的治疗方法。我们研究了大鼠海马脑片CA 3-CA 1突触的可塑性。长时程增强（LTP）的突触传递明显受损，而长时程抑制（LTD）增强，48小时后TBI相比，未手术和假手术对照组大鼠。脑外伤后给予环孢菌素A，一种稳定线粒体功能的化合物，导致LTP损伤的显著改善，并完全阻止了LTD的增强。我们的数据表明，海马突触可塑性的改变可能是脑外伤导致学习和记忆障碍的原因，而环孢菌素A等稳定线粒体功能的药物可能是脑外伤的有效治疗方法。(C)北京大学出版社.
Although traumatic brain injury (TBI) often results in impaired learning and memory functions, the underlying mechanisms are unknown and there are currently no treatments that can preserve such functions. We studied plasticity at CA3-CA1 synapses in hippocampal slices from rats subjected to controlled cortical impact TBI. Long-term potentiation (LTP) of synaptic transmission was markedly impaired, whereas long-term depression (LTD) was enhanced, 48 h following TBI when compared to unoperated and sham control rats. Post-TBI administration of cyclosporin A, a compound that stabilizes mitochondrial function, resulted in a highly significant amelioration of the impairment of LTP and completely prevented the enhancement of LTD. Our data suggest that alterations in hippocampal synaptic plasticity may be responsible for learning and memory deficits resulting from TBI and that agents such as cyclosporin A that stabilize mitochondrial function may be effective treatments for TBI. (C) 2000 Academic Press.