Yamaguchi T, Kato M, Fukui M, Akazawa K
Department of Clinical Neurophysiology, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Brain Res. 1992 Dec 11;598(1-2):38-44. doi: 10.1016/0006-8993(92)90165-6.
In order to elucidate the neuronal mechanism of the motor disturbances of the Rolling mouse Nagoya (rolling), a neurological mutant mouse (genotype rol/rol) showing frequent lurching and falling over on walking, we determined absolute rates of local cerebral glucose utilization (LCGU) with the [14C]deoxyglucose method. The rates were compared with those of heterozygote (+/rol) with normal behavior, and of normal mice (+/+) of the same strain (C3Hf/Nga). Rolling showed marked and significant increases in LCGU in the structures of the basal ganglia such as the globus pallidus, entopeduncular nucleus, substantia nigra pars compacta and pars reticulata, and subthalamic nucleus, confirming our previous finding with semiquantitative LCGU determination. Additional significant but much less marked increases in LCGU of rolling were found in some structures of the brainstem and limbic system, such as the pedunculopontine nucleus, red nucleus, ventral tegmental area, lateral habenula, and CA1 and CA3 of the hippocampus. Although rolling has been regarded as an animal model of cerebellar ataxia, rolling showed no alterations of LCGU in the cerebellum. The heterozygote showed intermediate increases in LCGU between rolling and normal mice in the basal ganglia structures such as the globus pallidus, substantia nigra pars reticulata and subthalamic nucleus. Our findings indicate that rolling has a definite, genetically determined dysfunction of the basal ganglia. The primary site of the basal ganglia dysfunction might probably be in the striatum, involving both the neostriatum and limbic striatum, and resulting in secondary dysfunction in their target structures.
为了阐明滚动小鼠名古屋品系（Rolling mouse Nagoya，rolling）运动障碍的神经元机制，该品系是一种神经学突变小鼠（基因型rol/rol），行走时频繁出现突然倾斜和摔倒的情况，我们采用[14C]脱氧葡萄糖法测定了局部脑葡萄糖利用率（LCGU）的绝对速率。将这些速率与行为正常的杂合子（+/rol）以及同一品系（C3Hf/Nga）的正常小鼠（+/+）的速率进行了比较。Rolling小鼠在基底神经节结构如苍白球、内囊核、黑质致密部和网状部以及丘脑底核中，LCGU显著增加，这证实了我们之前用半定量LCGU测定法得到的结果。在Rolling小鼠中，脑干和边缘系统的一些结构如脚桥核、红核、腹侧被盖区、外侧缰核以及海马的CA1和CA3区，LCGU也有显著但程度较轻的增加。尽管Rolling小鼠一直被视为小脑共济失调的动物模型，但在小脑中其LCGU并无改变。杂合子在基底神经节结构如苍白球、黑质网状部和丘脑底核中的LCGU增加程度介于Rolling小鼠和正常小鼠之间。我们的研究结果表明，Rolling小鼠存在明确的、由基因决定的基底神经节功能障碍。基底神经节功能障碍的主要部位可能在纹状体，包括新纹状体和边缘纹状体，并导致其靶结构的继发性功能障碍。
