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在缺乏NMDA受体亚基ε1的突变小鼠中,长痕迹间隔眨眼条件反射受损。

Long-trace interval eyeblink conditioning is impaired in mutant mice lacking the NMDA receptor subunit epsilon 1.

作者信息

Kishimoto Y, Kawahara S, Mori H, Mishina M, Kirino Y

机构信息

Laboratory of Neurobiophysics, School of Pharmaceutical Sciences, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan.

出版信息

Eur J Neurosci. 2001 Mar;13(6):1221-7. doi: 10.1046/j.0953-816x.2001.01486.x.

DOI:10.1046/j.0953-816x.2001.01486.x
PMID:11285019
Abstract

To elucidate the role of the N-methyl-D-aspartate (NMDA) -type glutamate receptor subunit epsilon 1 (GluR epsilon 1) in classical eyeblink conditioning, delay and trace eyeblink conditioning were investigated in GluR epsilon 1-null mutant mice. In delay conditioning and short-trace interval conditioning with a trace interval of 250 ms, GluR epsilon 1 mutant mice attained a normal level of the conditioned response (CR), although acquisition was a little slower than in wild-type mice. In contrast, GluR epsilon 1 mutant mice exhibited severe impairment of the attained level of the CR and disturbed temporal pattern of CR expression in trace conditioning with a longer trace interval of 500 ms. These findings indicate that GluR epsilon 1 is essential for long-trace interval eyeblink conditioning. The impairments of the associative learning with a long temporal separation between the conditioned and unconditioned stimuli observed in the GluR epsilon 1 mutant mice could be attributed to an impairment of hippocampal long-term potentiation in this line of mutant mice.

摘要

为阐明N-甲基-D-天冬氨酸(NMDA)型谷氨酸受体亚基ε1(GluRε1)在经典眨眼条件反射中的作用,我们对GluRε1基因敲除突变小鼠进行了延迟性和痕迹性眨眼条件反射研究。在延迟性条件反射和痕迹间隔为250毫秒的短痕迹间隔条件反射中,尽管GluRε1突变小鼠的习得过程比野生型小鼠稍慢,但它们的条件反应(CR)水平达到了正常水平。相比之下,在痕迹间隔为500毫秒的较长痕迹间隔的痕迹性条件反射中,GluRε1突变小鼠表现出CR水平严重受损以及CR表达的时间模式紊乱。这些发现表明,GluRε1对于长痕迹间隔眨眼条件反射至关重要。在GluRε1突变小鼠中观察到的条件刺激和非条件刺激之间存在长时间间隔时联想学习的损伤,可能归因于该品系突变小鼠海马长时程增强的损伤。

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