Fujii S, Kato H, Kuroda Y
Department of Physiology, Yamagata University School of Medicine, Japan.
Neurosci Lett. 1999 Nov 26;276(1):21-4. doi: 10.1016/s0304-3940(99)00776-4.
The mechanism of adenosine 5'-triphosphate (ATP)-induced long-term potentiation (LTP) was studied pharmacologically using guinea pig hippocampal slices. Application of 10 microM ATP for 10 min transiently depressed, then slowly augmented, synaptic transmission in CA1 neurons, leading to LTP. This ATP-induced LTP was blocked by addition of an N-methyl-D-aspartate (NMDA) glutamate receptor antagonist. Furthermore, co-application of 10 microM ATP and 100 microM L-glutamate for 10 min also induced LTP, and this effect was blocked by the use of Ca2+-free solution during drug application. These results suggest that, in CA1 neurons, a co-operative effect involving extracellular ATP and the activation of NMDA receptors, which increases intracellular Ca2+ levels, is required to trigger the intracellular biological process involved in ATP-induced LTP.
利用豚鼠海马切片，从药理学角度研究了三磷酸腺苷（ATP）诱导的长时程增强（LTP）机制。施加10微摩尔ATP 10分钟，会使CA1神经元的突触传递先短暂抑制，然后缓慢增强，从而导致LTP。这种ATP诱导的LTP可通过添加N-甲基-D-天冬氨酸（NMDA）谷氨酸受体拮抗剂来阻断。此外，共同施加10微摩尔ATP和100微摩尔L-谷氨酸10分钟也可诱导LTP，且在药物施加期间使用无钙溶液可阻断此效应。这些结果表明，在CA1神经元中，触发ATP诱导LTP所涉及的细胞内生物学过程需要细胞外ATP和NMDA受体激活的协同作用，这种协同作用会增加细胞内钙离子水平。
