Alterations of Spontaneous Behaviors and the Neuronal Activities of the Deep Cerebral Nuclei by Subthalamic Lesion with Kainic Acid in Rat Parkinsonian Models with 6-hydroxydopamine.

Chang, Jong Hee; Park, Yong Sook; Jeon, Mi Fa; Chang, Jin Woo; Park, Yong Gou; Chung, Sang Sup

Original Article

Journal of Korean Neurosurgical Society 2004;35(6): 605-613.

Jong Hee Chang, Yong Sook Park, Mi Fa Jeon, Jin Woo Chang, Yong Gou Park, Sang Sup Chung

¹Department of Neurosurgery, Yonsei University College of Medicine, Seoul, Korea. jchang@yumc.yonsei.ac.kr
²Medical Research Center, Yonsei University College of Medicine, Seoul, Korea.
³Brain Research Institute, Yonsei University College of Medicine, Seoul, Korea.
⁴BK21 Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea.

ABSTRACT

OBJECTIVE
The purpose of this study is to investigate the effect of ipsilateral subthalamic nucleus(STN) lesioning on the spontaneous behavioral changes and the alteration of neuronal activities of deep cerebral nuclei in the rat parkinsonian model with 6-hydroxydopamine(6-OHDA). METHODS: To identify the spontaneous behavioral changes, apomorphine-induced rotational test and forepaw adjusting step were performed. We subsequently investigated the alteration of neuronal activities in the substantia nigra pars reticulata(SNpr) and globus pallidus(GP), in order to compare them with the behavioral changes in rat parkinsonian models. RESULTS: The STN lesioning in the rat parkinsonian model clearly improved behavioral changes. Compared to the normal control rats, rat PD models exhibited a significant increase in mean firing rates and the percentage of bursting neurons in the STN and SNpr. In the STN-lesioned rat PD models, mean firing rates and the percentage of bursting neurons in the SNpr were reduced and those in the GP increased. CONCLUSION: STN lesioning induced behavior improvement in rat parkinsonian models seems to be consistent with the surgical outcomes of the STN stimulation therapy in advanced Parkinsonn's disease(PD). The alteration of the neuronal activities in the SNpr and GP suggests that these sites are responsible for the improvement of parkinsonian motor symptoms observed following STN lesioning in rat parkinsonian models. The significance of bursting activity in the SNpr and GP remains obscure. Further study is necessary to elucidate the pathophysiological mechanism of PD.