Kaneda Katsuyuki, Imanishi Michiko, Nambu Atsushi, Shigemoto Ryuichi, Takada Masahiko
Department of System Neuroscience, Tokyo Metropolitan Institute for Neuroscience, Tokyo Metropolitan Organization for Medical Research, Fuchu, Tokyo 183-8526, Japan.
Neuroreport. 2003 May 23;14(7):947-50. doi: 10.1097/01.wnr.0000074344.81633.e4.
The expression pattern of metabotropic glutamate receptor 1alpha (mGluR1alpha) was immunohistochemically investigated in substantia nigra dopaminergic neurons of the macaque monkey. In normal monkeys, mGluR1alpha immunoreactivity was weakly observed in the dorsal tier of the substantia nigra pars compacta (SNc-d) where calbindin-D28k-containing dopaminergic neurons invulnerable to parkinsonian degeneration are specifically located. On the other hand, mGluR1alpha was strongly expressed in the ventral tier of the substantia nigra pars compacta (SNc-v). In monkeys treated with the parkinsonism-inducing drug, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), mGluR1alpha expression was decreased in dopaminergic neurons in the SNc-v that were spared its toxic action. These results suggest that mGluR1alpha expression may be involved at least partly in the vulnerability of dopaminergic neurons to parkinsonian insults.
运用免疫组织化学方法，对猕猴黑质多巴胺能神经元中代谢型谷氨酸受体1α（mGluR1α）的表达模式进行了研究。在正常猴子中，黑质致密部背侧层（SNc-d）中可微弱观察到mGluR1α免疫反应性，而对帕金森病性退变具有抵抗力的、含钙结合蛋白-D28k的多巴胺能神经元就特异性地位于此处。另一方面，mGluR1α在黑质致密部腹侧层（SNc-v）中强烈表达。在用诱发帕金森病的药物1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）处理的猴子中，SNc-v中未受其毒性作用影响的多巴胺能神经元的mGluR1α表达降低。这些结果表明，mGluR1α的表达可能至少部分参与了多巴胺能神经元对帕金森病性损伤的易感性。
