| Parkinson's disease (PD) is a chronic progressive neurodegener -ative disease among middle age and old-age persons. Clinically, PD is characterized by tremor, rigidity, bradykinesia and postural instability. The principal neuropathological characteristic of PD is degeneration of dopamine neurons in the substantia nigra pars compacta and the substantia nigrostriatal pathway. The episode rate of PD increased year by year as the course of population aging. Motor disability caused by PD burden on families and society. Therefore, the study of PD became one of primary concerns of people day by day.The most valuable model of PD available at present is the monkey model treated with l-methyl-4-phenyl-l,2,3,6-tetra -hydropyridine (MPTP). It can reproduce virtually all the classic behavioural, biochemical, and pathological changes that occur in human PD, frequently used to study PD. Therefore, in the presentstudy, two rhesus monkeys were rendered hemiparkinsonian byinjecting MPTP unilaterally through the common carotid artery into the internal carotid artery after temporarily clamping the ipsilateral external carotid artery, animals' behaviour was observed and evaluation. The pathological changes of the substantia nigra and striatum in one normal control monkey and two monkeys lesioned by MPTP were observed by using HE stained, Nissl stained, TH-immunohistochemstry , GFAP-immunohistochemistry, and transmission electron microscope. The results demonstrate that two monkeys lesioned by MPTP developed hemiparkinsonian symptoms, showed the rotation towards contralateral to the side of the lesion after the administration of apomorphine, the score on the Benazzouz clinical rating scale reached 8, and the motor behaviour has been improved by the administration of Madopar. The pathologic changes of the substantia nigra and striatum in the MPTP lesioned side were found, which included the degeneration and death of neurons in HE stained sections, the significant decrement of Nissl-positive neurons, the significant decrement of TH-positive neurons and fibers, and the significant increment of GFAP-positive cells. The changes of ultrastructure of the substantia nigra and striatum in the MPTP lesioned side were also found, which included swelling and partial vacuoles of mitochondria, dilation of granular endoplasmic reticulum and Golgi complex, increment of lipofuscin, and hyperplasia of astrocyte. Moreover, the similar slight changes were also found in the substantia nigra and striatum contralateral to the MPTP lesioned side. According to the results, we might draw to the conclusions: hemiparkinsonian monkey models were successfully induced by injecting MPTP unilaterally into the internal carotid artery after temporarily clamping the ipsilateral external carotidartery.The pathogenesis of PD has yet to be clarified. However, mitochondrial complex I dysfunction and free radical-mediated oxidative stress metabolism are critical components of most current theories of pathogenesis in PD. Microtubule associated protein 2 (MAP-2) as a cytoskeleton protein, is localized primarily in neuronal dendrites and is known to stabilize microtubule assembly and maintain neuroarchitecture and mediate mitochondrial transport through axon. Moreover, MAP-2 is closely related to mitochondria in the structure and function. Yet, whether PD can be induced by the degeneration and death of neurons in the substantia nigra and striatum secondary to damaged MAP-2 and microtubule system of neurons due to mitochondrial complex I dysfunction? Nitric oxide (NO) is one of the production of free radicals-mediated oxidative stress. The excessive production of NO may contribute to neuronal degeneration and death. Nitric oxide synthase(NOS) is a key factor for synthesizing NO. Yet, whether the increment of NOS inducing the excessive production of NO could be involved in the mechanism of neuronal degeneration and death of the substantia nigra and striatum in PD? Therefore, in the present study, the changes of HMW MAP-2- positive fibers and NOS-posi...
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