Excitotoxic lesions of the pedunculopontine tegmental nucleus produce contralateral hemiparkinsonism in the monkey

被引:111
作者
Kojima, J
Yamaji, Y
Matsumura, M
Nambu, A
Inase, M
Tokuno, H
Takada, M
Imai, H
机构
[1] KYOTO UNIV,FAC MED,DEPT MORPHOL BRAIN SCI,KYOTO 60601,JAPAN
[2] JUNTENDO UNIV,SCH MED,DEPT NEUROL,TOKYO 113,JAPAN
[3] SAYAMA NEUROL HOSP,DEPT NEUROL,SAYAMA,SAITAMA 35013,JAPAN
[4] JUNTENDO UNIV,SCH MED,DEPT PUBL HLTH,TOKYO 113,JAPAN
[5] GUNMA UNIV,SCH MED,DEPT NEUROSURG,MAEBASHI,GUMMA 371,JAPAN
[6] TOKYO METROPOLITAN INST NEUROSCI,DEPT NEUROBIOL,FUCHU,TOKYO 183,JAPAN
[7] ELECTROTECH LAB,MOL & CELLULAR NEUROSCI SECT,TSUKUBA,IBARAKI 305,JAPAN
关键词
pedunculopontine tegmental nucleus; nigrostriatal neuron; parkinsonism; dopamine; excitatory input; acetylcholine; glutamate; monkey;
D O I
10.1016/S0304-3940(97)00254-1
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Dopaminergic nigrostriatal neurons, degeneration of which causes Parkinson's disease, are known to receive excitatory input almost exclusively from the pedunculopontine tegmental nucleus (PPN). We report here that excitotoxic lesions of the PPN produce abnormal motor signs relevant to hemiparkinsonism in the macaque monkey. Under the guidance of extracellular unit recordings, the electrophysiologically identified PPN was injected unilaterally with kainic acid. These PPN-lesioned monkeys exhibited mild to moderate levels of flexed posture and hypokinesia in the upper and lower limbs contralateral to the lesion. In most of the monkeys, such pathophysiological events were gradually improved and became stationary in 1-2 weeks. The hemiparkinsonian symptoms observed after PPN destruction might be ascribed to a decrease in nigrostriatal neuron activity due to excitatory input ablation. (C) 1997 Elsevier Science Ltd.
引用
收藏
页码:111 / 114
页数:4
相关论文
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