Department of Psychiatry and Psychotherapy, RG Animal Models in Psychiatry, Central Institute of Mental Health, Medical Faculty Mannheim, University of Heidelberg, J 5, 68159, Mannheim, Germany,
J Neural Transm (Vienna). 2013 Nov;120(11):1605-9. doi: 10.1007/s00702-013-1049-2. Epub 2013 Jun 5.
The glutamate hypothesis of schizophrenia postulates NMDA receptor hypofunction as important pathophysiological mechanism. In rodents, NMDA receptor antagonists induce together with psychosis-like effects cortical injury. Stress during adolescence can trigger schizophrenia by unknown mechanisms. Here we show in rats that juvenile chronic isolation significantly increases MK-801-triggered expression of heat shock protein 70, a marker of neuronal injury, in the retrosplenial cortex. These data suggest an additive effect of juvenile stress and NMDA receptor blockade, with possible relevance for schizophrenia.
精神分裂症的谷氨酸假说假设 NMDA 受体功能低下是重要的病理生理机制。在啮齿动物中，NMDA 受体拮抗剂与类精神病作用一起诱导皮质损伤。青春期的应激可能通过未知机制引发精神分裂症。在这里，我们在大鼠中表明，青少年慢性隔离会显着增加 MK-801 引发的热休克蛋白 70 的表达，热休克蛋白 70 是神经元损伤的标志物，在扣带回后皮质中。这些数据表明青少年应激和 NMDA 受体阻断的附加效应，可能与精神分裂症有关。
