Morphologic changes within the cerebellar cortex in the unilateral 6-hydroxydopamine lesioned rat model for Parkinson disease

Abstract

Parkinson’s disease (PD) is a common neurodegenerative disorder caused by the progressive loss of dopaminergic neurons in the substantia nigra. Most investigations have focused on the cerebral regions such as the basal ganglia, thalamus, or the substantia nigra, but whether there is pathologic impairment within the cerebellum has rarely been assessed. Synapsin and neurofilament as the inner markers of neurons and synapses reflect the functional state by their distribution or expression. Significant morphologic changes at the cellular level have been demonstrated directly or indirectly in multiple neurodegenerative diseases. The purpose of this study was to determine whether the behavioral abnormalities that accompany PD are associated with the cerebellum using an in vivo 6- hydroxydopamine lesioned rat model. Forty-two rats were divided into three groups, the Parkinsonian group (N=22), sham group (N=10) and control group (N=10). The dopaminergic lesion was determined by immunohistochemical analysis for tyrosine hydroxylaseimmunopositive cells. Immunohistochemical studies showed that the density of synapsin I in the granular layer of the cerebellum on both sides of the Parkinsonian -model was not statistically significantly different compared to the control and sham groups. However, expression of neurofilament H in the cortex within bilateral paramedian lobule (PML) and Crus 2 of the ansiform lobule (C2AL) in cerebellum posterior lobe of Parkinsonian rats was decreased compared with controls (P<0.05), especially in the loss of Purkinje cells and the presence of morphologic abnormalities in the cell nucleus. The study suggested that loss of neurons and synapses may take place in the cerebellar cortex of Parkinson’s disease, and might play an important role in the pathologic mechanism of PD.