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缺乏δ2谷氨酸受体亚基的突变小鼠前庭代偿延迟。

Retarded vestibular compensation in mutant mice deficient in delta 2 glutamate receptor subunit.

作者信息

Funabiki K, Mishina M, Hirano T

机构信息

Department of Physiology, Kyoto University, Japan.

出版信息

Neuroreport. 1995 Dec 29;7(1):189-92.

PMID:8742448
Abstract

The delta 2 subunit of ionotropic glutamate receptors is expressed only in the cerebellar Purkinje cell. In mutant mice deficient in the delta 2 protein, cerebellar long-term depression and motor coordination are impaired. We examined behavioural plasticity in these mutant mice after unilateral vestibular destruction. After intratympanic injection of sodium arsanilate, the mice showed roll head tilt and their righting response under a rotation load was impaired. These symptoms improved with time. However, compensation of the righting response was retarded in the mutant mice. These results suggest that motor learning of the delta 2 mutant mice is disturbed, and that the static and dynamic components of vestibular compensation may be controlled by different neuronal mechanisms.

摘要

离子型谷氨酸受体的δ2亚基仅在小脑浦肯野细胞中表达。在缺乏δ2蛋白的突变小鼠中,小脑长时程抑制和运动协调受损。我们检查了这些突变小鼠单侧前庭破坏后的行为可塑性。经鼓室内注射对氨基苯胂酸钠后,小鼠出现头部滚动倾斜,其在旋转负荷下的翻正反应受损。这些症状随时间改善。然而,突变小鼠的翻正反应补偿延迟。这些结果表明,δ2突变小鼠的运动学习受到干扰,并且前庭补偿的静态和动态成分可能由不同的神经元机制控制。

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