OBJECT: The purpose of this study was to investigate the spontaneous behavioral changes and the alteration of neuronal activities in the pedunculopontine nucleus (PPN) after ipsilateral subthalamic nucleus (STN) lesioning by kainic acid in a rat parkinsonian model created by lesioning with 6-hydroxydopamine (6-OHDA). METHODS: Assumptions about the mechanisms mediating the effects of lesioning of the nigrostriatal dopaminergic pathway by 6-OHDA and the effects of STN lesioning were examined behaviorally by means of apomorphine-induced rotational behavior and forepaw-adjusting steps. The authors subsequently investigated the alteration of neuronal activities in the PPN to compare them with the behavioral changes in rat parkinsonian models. CONCLUSIONS: The results demonstrated that STN lesioning induced behavioral improvement in rat parkinsonian models. This result, which confirms previously held assumptions, may account for the therapeutic effect of STN stimulation in Parkinson disease. The alteration of the neuronal activities in the PPN units also indicates that the PPN units are responsible for the improvement in motor symptoms observed after STN lesioning in rat parkinsonian models.
OBJECT: The purpose of this study was to investigate the spontaneous behavioral changes and the alteration of neuronal activities in the pedunculopontine nucleus (PPN) after ipsilateral subthalamic nucleus (STN) lesioning by kainic acid in a ratparkinsonian model created by lesioning with 6-hydroxydopamine (6-OHDA). METHODS: Assumptions about the mechanisms mediating the effects of lesioning of the nigrostriatal dopaminergic pathway by 6-OHDA and the effects of STN lesioning were examined behaviorally by means of apomorphine-induced rotational behavior and forepaw-adjusting steps. The authors subsequently investigated the alteration of neuronal activities in the PPN to compare them with the behavioral changes in ratparkinsonian models. CONCLUSIONS: The results demonstrated that STN lesioning induced behavioral improvement in ratparkinsonian models. This result, which confirms previously held assumptions, may account for the therapeutic effect of STN stimulation in Parkinson disease. The alteration of the neuronal activities in the PPN units also indicates that the PPN units are responsible for the improvement in motor symptoms observed after STN lesioning in ratparkinsonian models.
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