Ben-Ari Y, Krnjević K, Crépel V
INSERM U. 29, Hôpital de Port-Royal, Paris, France.
Neuroscience. 1990;37(1):55-60. doi: 10.1016/0306-4522(90)90191-6.
In CA3 hippocampal neurons of the rat, brief anoxic episodes produce a depolarization which is probably due to a synaptic release of glutamate. Diazoxide, an activator of ATP-sensitive K+ channels (K+ ATP), blocks the anoxic depolarization and has no effect in control oxygenated artificial cerebrospinal fluid. The hormone somatostatin which activates K+ ATP channels in the pancreas also reduces the anoxic depolarization in CA3 neurons. We suggest that drugs that open K+ ATP channels may constitute a novel approach to selectivity reducing the deleterious effects of excessive release of glutamate during anoxia without producing a generalized blockade of glutamatergic synaptic transmission.
在大鼠的CA3海马神经元中，短暂的缺氧发作会产生去极化，这可能是由于谷氨酸的突触释放所致。二氮嗪是一种ATP敏感性钾通道（K⁺ATP）的激活剂，它能阻断缺氧去极化，而在对照的含氧人工脑脊液中则没有作用。激活胰腺中K⁺ATP通道的激素生长抑素也能减少CA3神经元中的缺氧去极化。我们认为，打开K⁺ATP通道的药物可能构成一种新的方法，可选择性地减少缺氧期间谷氨酸过度释放的有害影响，而不会导致谷氨酸能突触传递的普遍阻断。
