Maren S, Baudry M, Thompson R F
Neurosciences Program, University of Southern California, Los Angeles 90089-2520.
Synapse. 1992 Jul;11(3):221-8. doi: 10.1002/syn.890110307.
The effects of the novel competitive N-methyl-D-aspartate (NMDA) receptor antagonist, CGP 39551 [the carboxyethylester of CGP 37849; DL-(E)-2-amino-4-methyl-5-phosphono-3-pentenoic acid], on extracellular field potentials and long-term potentiation (LTP) induced in the dentate gyrus by stimulation of the perforant path were studied in anesthetized rats. CGP 39551 attenuated the population spike (PS) and excitatory postsynaptic potential (EPSP) amplitude of dentate field potentials, reduced the NMDA receptor-mediated component of train-evoked burst potentials, and prevented the induction of LTP. The decrease in PS and EPSP amplitude produced by CGP 39551 was observed mainly in non-potentiated synaptic populations; potentiated field potentials were only minimally affected by drug treatment. These results are consistent with receptors may contribute in a tonic manner to the state of dentate granule cell excitability. Finally, the differential modulation of potentiated and non-potentiated synapses by CGP 39551 suggests that a change in some properties of postsynaptic AMPA receptors is involved in the expression of LTP.
在麻醉大鼠中，研究了新型竞争性N-甲基-D-天冬氨酸（NMDA）受体拮抗剂CGP 39551 [CGP 37849的羧乙酯；DL-(E)-2-氨基-4-甲基-5-膦酰基-3-戊烯酸] 对穿通路径刺激诱导的齿状回细胞外场电位和长时程增强（LTP）的影响。CGP 39551减弱了齿状场电位的群体峰电位（PS）和兴奋性突触后电位（EPSP）幅度，降低了强直刺激诱发的爆发电位中NMDA受体介导的成分，并阻止了LTP的诱导。CGP 39551引起的PS和EPSP幅度降低主要在未增强的突触群体中观察到；增强的场电位仅受到药物治疗的轻微影响。这些结果与受体可能以紧张性方式对齿状颗粒细胞兴奋性状态有贡献一致。最后，CGP 39551对增强和未增强突触的差异调节表明，突触后AMPA受体某些特性的变化参与了LTP的表达。
