Clifford D B, Zorumski C F, Olney J W
Department of Neurology, Washington University School of Medicine, St. Louis, Missouri 63110.
Exp Neurol. 1989 Sep;105(3):272-9. doi: 10.1016/0014-4886(89)90130-1.
Ketamine and MK-801 act at phencyclidine receptors to block transmitter activity through the N-methyl-D-aspartate (NMDA) subtype of glutamate (GLU) receptor. These agents also block the potent excitotoxic actions of NMDA and are of interest for their potential ability to protect against neurodegenerative processes mediated by the excitotoxic action of endogenous Glu at NMDA receptors. Here we show that degeneration of thalamic neurons caused by persistent seizure activity in the corticothalamic tract (putative glutamergic transmitter pathway) is prevented by systemic administration of ketamine or MK-801, despite the failure of these agents to eliminate persistent electrographic seizure activity recorded from cortex and thalamus.
氯胺酮和MK-801作用于苯环己哌啶受体，通过谷氨酸（GLU）受体的N-甲基-D-天冬氨酸（NMDA）亚型来阻断递质活性。这些药物还能阻断NMDA的强效兴奋性毒性作用，因其具有潜在能力保护机体免受内源性谷氨酸在NMDA受体处的兴奋性毒性作用所介导的神经退行性过程影响而备受关注。在此我们表明，尽管氯胺酮或MK-801未能消除从皮层和丘脑记录到的持续性脑电图癫痫活动，但通过全身给药可预防由皮质丘脑束（假定的谷氨酸能递质通路）中持续性癫痫活动所导致的丘脑神经元变性。
