Abstract
The condition produced by the neurotoxin
1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in the nonhuman
primate clearly models the striatal and nigral dopamine deficiency
found in Parkinson's disease (PD). However, evidence supporting its
ability to mimic changes outside the nigrostriatal dopaminergic
system known to occur in the idiopathic disease is controversial.
In order to further assess the validity of the MPTP-treated monkey
model of PD, this study investigated the changes in the serotonin
and catecholamine cortical projections in nonhuman primates
rendered parkinsonian following chronic exposure to MPTP.
Quantitative analysis of immunohistochemical staining with
antibodies raised against tyrosine hydroxylase (TH) and serotonin
(5HT) in various cortical areas involved in cognitive, limbic and
motor functions was compared between normal and parkinsonian
animals. In normal monkeys, TH and serotonin-positive axons and
terminals densely innervated all cortical areas. However, in the
MPTP-treated monkeys a reduction of innervation for both
transmitter systems that ranged from 17.77 to 76.08 % of control
values was found in all cortical regions, but the most striking
denervation was found in limbic and motor areas for TH and in the
motor areas for serotonin. These findings demonstrate that the
pathology of monoamine networks in the MPTP-treated nonhuman
primate as a model for PD extends beyond the nigrostriatal
dopaminergic system.
Table of Contents
Table of Contents
Introduction...1
Materials and Method...8
Results...12
Discussion...13
References...20
Table 1...29
Table 2...30
Table 3...31
Figure 1...32
Figure 2...33
Figure 3...34
Figure 4...35
Figure 5...36
Figure 6...37
Figure 7...38
Figure 8...39
Figure 9...40
Figure 10...41
Figure 11...42
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