Wu JianQun, Rowan Michael J, Anwyl Roger
Department of Physiology, Trinity College, Dublin 2, Ireland.
Neuropharmacology. 2004 Mar;46(3):311-7. doi: 10.1016/j.neuropharm.2003.09.014.
The induction of long-term potentiation (LTP) under conditions of blockade of the N-methyl-D-aspartate receptor (NMDAR) was studied in the medial perforant path to granule cell synapse in the dentate gyrus. A small amplitude NMDAR-independent potentiation was induced by a single brief high frequency stimulation (HFS), and a summated larger LTP was induced by repeated spaced HFS. The NMDAR-independent LTP was mediated by activation of group II mGluR as it was inhibited by the group II antagonists EGLU and also low concentrations of LY341495, but not the group I mGluR antagonist MPEP. Perfusion of the group II mGluR agonist DCG-IV induced NMDAR-independent LTP in media containing an NMDAR antagonist. The NMDAR-independent LTP induced by HFS was mediated via activation of p42/44 MAP kinase as it was blocked by the selective inhibitor PD98059.
在齿状回颗粒细胞突触的内侧穿通通路中，研究了在N-甲基-D-天冬氨酸受体（NMDAR）阻断条件下长时程增强（LTP）的诱导。单次短暂高频刺激（HFS）可诱导出小幅度的非NMDAR依赖性增强，重复间隔HFS可诱导出总和更大的LTP。非NMDAR依赖性LTP由II组代谢型谷氨酸受体（mGluR）的激活介导，因为它受到II组拮抗剂EGLU以及低浓度LY341495的抑制，但不受I组mGluR拮抗剂MPEP的抑制。在含有NMDAR拮抗剂的培养基中，灌注II组mGluR激动剂DCG-IV可诱导出非NMDAR依赖性LTP。HFS诱导的非NMDAR依赖性LTP通过p42/44丝裂原活化蛋白激酶（MAP激酶）的激活介导，因为它被选择性抑制剂PD98059阻断。
