Glebov R N, Golenda A M, Kryzhanovskiĭ G N
Biull Eksp Biol Med. 1979 Mar;87(3):204-7.
It was shown that the phenomenon of inactivation of Na, K-ATPase of the non-purified fraction of the rat cortical synaptosomes under electroshock may be related to "modification" of the potassium active center of the enzyme. The anticonvulsant diazepam injected intramuscularly also inhibits Na, K-ATPase of the cerebral membranes. However, in subsequent electrical stimulation of the brain the drug activates Na, K-ATPase as compared to controls. Diazepam also abolishes clonic convulsions induced by electrical stimulation of the brain. At the same time it does not eliminate compensatory shifts in the activity of acetyl-cholinesterase of the rat cerebral and spinal synaptosomes, characteristic of electroshock. The results are discussed from the standpoint that inhibition of the activity of Na, K-ATPase of the nerve endings membranes may underlie the pathogenetic mechanism of the convulsive activity.
结果表明，大鼠皮层突触体非纯化组分的钠钾 - ATP酶在电休克作用下的失活现象，可能与该酶钾活性中心的“修饰”有关。肌肉注射抗惊厥药物地西泮也会抑制脑膜的钠钾 - ATP酶。然而，在随后的脑电刺激中，与对照组相比，该药物会激活钠钾 - ATP酶。地西泮还能消除脑电刺激诱发的阵挛性惊厥。同时，它不会消除电休克所特有的大鼠脑和脊髓突触体乙酰胆碱酯酶活性的代偿性变化。从神经末梢膜钠钾 - ATP酶活性的抑制可能是惊厥活动发病机制基础的角度对结果进行了讨论。
