Shors T J, Servatius R J
Department of Psychology, Princeton University, NJ 08544-1010, USA.
Neuroreport. 1995 Mar 7;6(4):677-80. doi: 10.1097/00001756-199503000-00023.
Exposure to an inescapable stressor facilitates acquisition of a classically-conditioned eyeblink response in the freely-moving rat. Here, we tested the hypothesis that the facilitation is mediated via activation of the N-methyl-D-aspartate (NMDA) type of glutamate receptor. Rats were injected with the competitive NMDA antagonist CGP-37849 (5 mg kg-1) or vehicle 2 h prior to exposure to restraint and 90, 1 mA, 1 s tail shocks. In contrast to the dramatic facilitation exhibited in stressed rats injected with the vehicle, rats whose NMDA receptors were blocked during exposure to the stressor did not exhibit any facilitation 24 h later. The antagonist alone had no effect on learning. These results demonstrate that the stress-induced facilitation of classical conditioning is dependent on NMDA receptor activation and support the hypothesis that stress is inducing a phenomenon similar in mechanism to that of long-term potentiation (LTP).
暴露于不可逃避的应激源会促进自由活动大鼠获得经典条件性眨眼反应。在此，我们测试了以下假设：这种促进作用是通过激活N-甲基-D-天冬氨酸（NMDA）型谷氨酸受体介导的。在暴露于束缚和90次、1毫安、1秒的尾部电击前2小时，给大鼠注射竞争性NMDA拮抗剂CGP-37849（5毫克/千克）或溶剂。与注射溶剂的应激大鼠表现出的显著促进作用相反，在暴露于应激源期间NMDA受体被阻断的大鼠在24小时后未表现出任何促进作用。单独使用拮抗剂对学习没有影响。这些结果表明，应激诱导的经典条件作用促进依赖于NMDA受体激活，并支持以下假设：应激正在诱导一种机制与长时程增强（LTP）相似的现象。
