title: Functional changes in the frontal cortex in Parkinson's disease using a rat model.
abstract: In recent years, investigations of the pathologic mechanism of Parkinson's disease (PD) have mainly concentrated on the basal ganglia. However, recent studies have confirmed that pathological changes in PD are accompanied by functional motor changes of the cerebral cortex. Rats were injected with 6-hydroxydopamine and ascorbic acid in the right substantia nigra. In this rat model of PD, magnetic resonance spectroscopy showed the ratio of N-acetyl-aspartic acid to creatine in a lesion in the right frontal cortex was significantly lower than the same ratio in a control group of rats. The ratio of choline to creatine in a lesion in the right frontal cortex was not significantly different between the PD-model rats and control rats. In addition, the optical densities of neurofilament protein and synaptophysin positive sites decreased significantly on the side of the brain with the injury compared with the side without the injury, and with both sides in the control rats. The density of synapses in the frontal cortex on the lesioned side was decreased compared with the unlesioned side. There were abnormal changes in the presynaptic membrane, postsynaptic membrane and synaptic vesicles, and the typical synaptic structure was no longer apparent on the lesioned side. We hypothesized loss of neurons and synapses, abnormal synaptic structure and neuron and synaptic dysfunction of the frontal cortex with a lesion in the injury side of the frontal cortex in PD-model rats. These changes might have an important role in the pathologic mechanism of PD.
authors.affiliation: Department of Medical Imaging, Provincial Hospital Affiliated to Shandong University, Jinan, China.
authors.forename: Zhongyu
authors.initials: Z
authors.lastname: Hou
authors.forename: Hao
authors.initials: H
authors.lastname: Lei
authors.forename: Shuhui
authors.initials: S
authors.lastname: Hong
authors.forename: Bo
authors.initials: B
authors.lastname: Sun
authors.forename: Ke
authors.initials: K
authors.lastname: Fang
authors.forename: Xiangtao
authors.initials: X
authors.lastname: Lin
authors.forename: Maili
authors.initials: M
authors.lastname: Liu
authors.forename: David T W
authors.initials: DT
authors.lastname: Yew
authors.forename: Shuwei
authors.initials: S
authors.lastname: Liu
mesh_terms: D000818:Animals; D002452:Cell Count; D004195:Disease Models, Animal; D005625:Frontal Lobe / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D007150:Immunohistochemistry; D008279:Magnetic Resonance Imaging; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D046529:Microscopy, Electron, Transmission; D016900:Neurofilament Proteins / Q000378:metabolism; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D010300:Parkinson Disease / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D051381:Rats; D017208:Rats, Wistar; D013378:Substantia Nigra / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D013569:Synapses / Q000378:metabolism; D016708:Synaptophysin / Q000378:metabolism; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism
chemical_list: D016900:Neurofilament Proteins; D016708:Synaptophysin; D014446:Tyrosine 3-Monooxygenase