Excitotoxic lesions of the pedunculopontine tegmental nucleus produce contralateral hemiparkinsonism in the monkey
J Kojima, Y Yamaji, M Matsumura, A Nambu, M Inase… - Neuroscience …, 1997 - Elsevier
J Kojima, Y Yamaji, M Matsumura, A Nambu, M Inase, H Tokuno, M Takada, H Imai
Neuroscience letters, 1997•ElsevierDopaminergic 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 …
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 …
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.
Elsevier
