Pellmar T C
Physiology Department, Armed Forces Radiobiology Research Institute, Bethesda, MD 20889-5145.
Neuroscience. 1991;45(2):273-80. doi: 10.1016/0306-4522(91)90225-d.
A variety of fatty acids produced sustained changes in excitability in the guinea-pig hippocampal slice. Although each fatty acid was unique, a general pattern was evident. During a 30-min exposure, the synaptic potential was minimally affected, although population spike amplitude showed significant increases. With wash, synaptic efficacy increased. The increase in the synaptic potential was significant with arachidonic acid (100 microM), oleic acid (100 microM), myristic acid (250 microM) and capric acid (250 microM). Also with wash, the coupling between the synaptic potential and the population spike was reduced significantly for most of the fatty acids tested: arachidonic acid (50 microM, 100 microM), linoleic acid (100 microM) oleic acid (100 microM), stearic acid (100 microM), myristic acid (250 microM) and capric acid (250 microM, 500 microM). The fatty acids may influence neuronal excitability, in part, through a direct membrane action. The observed synaptic enhancement is consistent with a role for a fatty acid in long-term potentiation. In addition, fatty acid exposure mimics the effects of X-radiation. We suggest that free radical-induced release of fatty acids contributes to electrophysiological damage in a number of pathological states.
多种脂肪酸使豚鼠海马切片的兴奋性产生持续性变化。尽管每种脂肪酸都有其独特之处，但总体模式是明显的。在30分钟的暴露期间，突触电位受影响最小，尽管群体峰电位幅度有显著增加。洗脱后，突触效能增加。花生四烯酸（100微摩尔）、油酸（100微摩尔）、肉豆蔻酸（250微摩尔）和癸酸（250微摩尔）使突触电位显著增加。同样在洗脱后，对于大多数测试的脂肪酸，突触电位与群体峰电位之间的耦合显著降低：花生四烯酸（50微摩尔、100微摩尔）、亚油酸（100微摩尔）、油酸（100微摩尔）、硬脂酸（100微摩尔）、肉豆蔻酸（250微摩尔）和癸酸（250微摩尔、500微摩尔）。脂肪酸可能部分通过直接的膜作用影响神经元兴奋性。观察到的突触增强与脂肪酸在长时程增强中的作用一致。此外，脂肪酸暴露模拟了X射线辐射的效应。我们认为自由基诱导的脂肪酸释放导致了多种病理状态下的电生理损伤。
