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(±)CPP,一种N-甲基-D-天冬氨酸受体拮抗剂,可阻断麻醉大鼠中连合-海马体CA3长时程增强的诱导。

(+/-) CPP, an NMDA receptor antagonist, blocks the induction of commissural-CA3 LTP in the anesthetized rat.

作者信息

Hernandez R V, Derrick B E, Rodriguez W A, Martinez J L

机构信息

Department of Psychology, University of California, Berkeley 94720.

出版信息

Brain Res. 1994 Sep 5;656(1):215-9. doi: 10.1016/0006-8993(94)91388-9.

Abstract

Commissural CA3-CA3 (cCA3) long-term potentiation (LTP) was investigated in the anesthetized rat treated with the highly selective NMDA-receptor antagonist D,L-3[(+/-)-2-carboxypiperazin-4-yl]- propyl-1-phosphonic acid (CPP). Intraperitoneal injections of CPP did not significantly affect baseline test responses for either field EPSP slope or amplitude measures but did reduce LTP in a dose-dependent manner, with 3.2 mg/kg as the lowest effective dose. EPSP variability following tetanization was also significantly reduced in both the 3.2 mg/kg and 10.0 mg/kg groups. We interpret these results to suggest that a 3.2 mg/kg dose of CPP may be sufficient for studying the behavioral effects of this NMDA receptor antagonist.

摘要

在使用高选择性N-甲基-D-天冬氨酸(NMDA)受体拮抗剂D,L-3-[(+/-)-2-羧基哌嗪-4-基]-丙基-1-膦酸(CPP)处理的麻醉大鼠中,研究了连合CA3-CA3(cCA3)长时程增强(LTP)。腹腔注射CPP对场兴奋性突触后电位(EPSP)斜率或幅度测量的基线测试反应没有显著影响,但确实以剂量依赖的方式降低了LTP,3.2mg/kg为最低有效剂量。在3.2mg/kg和10.0mg/kg组中,强直刺激后的EPSP变异性也显著降低。我们将这些结果解释为表明3.2mg/kg剂量的CPP可能足以研究这种NMDA受体拮抗剂的行为效应。

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