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(RS)-α-甲基-4-羧基苯甘氨酸(MCPG)不会阻断大鼠海马切片CA1区的theta爆发诱导的长时程增强。

(RS)-alpha-methyl-4-carboxyphenylglycine (MCPG) does not block theta burst-induced long-term potentiation in area CA1 of rat hippocampal slices.

作者信息

Brown R E, Rabe H, Reymann K G

机构信息

Department of Neurophysiology, Institute for Neurobiology, Magdeburg, FRG.

出版信息

Neurosci Lett. 1994 Mar 28;170(1):17-21. doi: 10.1016/0304-3940(94)90228-3.

DOI:10.1016/0304-3940(94)90228-3
PMID:8041499
Abstract

We have used the selective metabotropic glutamate receptor antagonist (RS)-alpha-methyl-4-carboxyphenylglycine (MCPG) to investigate in the CA1 hippocampal subregion in vitro whether coactivation of N-methyl-D-aspartate (NMDA) and metabotropic glutamate receptors is necessary for the induction of long-term potentiation (LTP) when LTP is induced by theta burst stimulation (TBS). When MCPG (500 microM) was bath applied 14-30 min prior to a triple high-frequency tetanization (100 Hz, 1 s) and washed out immediately afterwards the potentiation of the extracellularly recorded field potentials decayed gradually to baseline (P < 0.05) over 2-3 h. However, when MCPG was applied in the same manner before a triple TBS (10 bursts at 5 Hz, 100 Hz within the bursts) the resulting potentiation remained stable for at least 4 h. MCPG had no effect on baseline synaptic transmission or post-tetanic potentiation. These results demonstrate a clear difference in the mechanisms underlying these two different forms of LTP.

摘要

我们使用了选择性代谢型谷氨酸受体拮抗剂(RS)-α-甲基-4-羧基苯基甘氨酸(MCPG),在体外海马CA1亚区研究当通过θ波爆发刺激(TBS)诱导长时程增强(LTP)时,N-甲基-D-天冬氨酸(NMDA)受体和代谢型谷氨酸受体的共同激活对于LTP诱导是否必要。当在三次高频强直刺激(100 Hz,1 s)前14 - 30分钟进行MCPG(500 microM)灌浴给药并随后立即洗脱时,细胞外记录的场电位增强在2 - 3小时内逐渐衰减至基线水平(P < 0.05)。然而,当在三次TBS(5 Hz的10个爆发,爆发内100 Hz)前以相同方式应用MCPG时,所产生的增强至少在4小时内保持稳定。MCPG对基线突触传递或强直后增强无影响。这些结果表明这两种不同形式LTP的潜在机制存在明显差异。

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