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목차
1. 서 론
2. 연구목적
3. 연구방법
4. 연구결과
5. 고 찰
6. 결 론
7. 참고문헌
8. 영문초록
2. 연구목적
3. 연구방법
4. 연구결과
5. 고 찰
6. 결 론
7. 참고문헌
8. 영문초록
본문내용
7
Weinshilboum RM, Thoa NB, Johnson DG, Kopin IJ, Axelrod J. Proportional release of norepinephrine and dopamine beta-hydroxylase from sympathetic nerves. Science 1971;174:1349-1351
Wilson, JM, Levey AI, Rajput A, et al. Differential changes in neurochemical markers of striatal dopamine nerve terminal in idiopathic Parkinson's disease. Neurology 1996;47:718-726
Yang-Feng TL, Xue F, Zhong W et al. Chromosomal organization of the adrenergic receptor genes. Proc Natl Acad Sci USA 1990;87:1516- 1520
Zigmond MJ, Stricker EM. Animal models of parkinsonism using selective neurotoxin: clinical and basic implication. Int Rev Neurobiol 1989;31: 1-79
Zhong X-H, Haycock JW, Shannak K, et al. striatal dihydroxyphenylalanine decarboxylase and tyrosine hydroxylase protein in idiopathic Parkinson's disease and dominantly inherited olivopontocerebellar atrophy. Mov Disord 1995;10:10-17
Abstract
In Parkinson's disease, the dopaminergic neurons of the substantia nigra are selectively destroyed and the consequent lack of dopamine in the striatum is responsible for the motor disturbances. Parkinsonian symptoms appear when the decrease in striatal dopamine is greater than 80%. However there are evidences that the nigral dopaminergic cell loss is less than dopamine decrease in the striatum.
Dopamine transporter is located on the presynaptic nerve terminal and plays an important physiological role in the inactivation and recycling of dopamine released into the synaptic cleft by actively pumping exrtacellular dopamine back into the terminal. Therefore dopamine transporter is considered to be a reliable marker of presynaptic dopaminergic terminal function in striatum. Preivious in vivo and postmortem radio-labelled ligand binding studies and postmortem quantitative immunoblotting studies have demonstrated a loss of dopamine transporter in the striatum of Parkinson's disease brain.
To examine whether the striatal nerve terminals have more severe destruction than nigral dopaminergic cell itself in the MPTP-treated mosue model of Parkinson's disease, the striatal dopamine and dopamine transporter were measured by HPLC and quantitative immunoblotting, respectively. The number of nigral dopaminergic cell was counted by immunohistochemical staining for tyrosine hydroxylase.
The degree of reduction in the level of striatal dopamine, in the level of striatal dopamine transporter and in the number of nigral dopaminergic cell correlated well. The degree of reduction in the level of striatal dopamine and striatal dopamine transporter was greater than the degree of reduction in the number of nigral dopaminergic cell.
This study shows that damage of the nerve cell body the substantia nigra is less severe than that of the nerve terminal in the striatum, which allows an opportunity for neuroprotective or halting therapeutic modalities in Parkinson's disease.
Key Words : Parkinson's disease, MPTP, mouse, dopaminergic cell,
dopamine transporter, western blot
Student Number : 91801-886
Weinshilboum RM, Thoa NB, Johnson DG, Kopin IJ, Axelrod J. Proportional release of norepinephrine and dopamine beta-hydroxylase from sympathetic nerves. Science 1971;174:1349-1351
Wilson, JM, Levey AI, Rajput A, et al. Differential changes in neurochemical markers of striatal dopamine nerve terminal in idiopathic Parkinson's disease. Neurology 1996;47:718-726
Yang-Feng TL, Xue F, Zhong W et al. Chromosomal organization of the adrenergic receptor genes. Proc Natl Acad Sci USA 1990;87:1516- 1520
Zigmond MJ, Stricker EM. Animal models of parkinsonism using selective neurotoxin: clinical and basic implication. Int Rev Neurobiol 1989;31: 1-79
Zhong X-H, Haycock JW, Shannak K, et al. striatal dihydroxyphenylalanine decarboxylase and tyrosine hydroxylase protein in idiopathic Parkinson's disease and dominantly inherited olivopontocerebellar atrophy. Mov Disord 1995;10:10-17
Abstract
In Parkinson's disease, the dopaminergic neurons of the substantia nigra are selectively destroyed and the consequent lack of dopamine in the striatum is responsible for the motor disturbances. Parkinsonian symptoms appear when the decrease in striatal dopamine is greater than 80%. However there are evidences that the nigral dopaminergic cell loss is less than dopamine decrease in the striatum.
Dopamine transporter is located on the presynaptic nerve terminal and plays an important physiological role in the inactivation and recycling of dopamine released into the synaptic cleft by actively pumping exrtacellular dopamine back into the terminal. Therefore dopamine transporter is considered to be a reliable marker of presynaptic dopaminergic terminal function in striatum. Preivious in vivo and postmortem radio-labelled ligand binding studies and postmortem quantitative immunoblotting studies have demonstrated a loss of dopamine transporter in the striatum of Parkinson's disease brain.
To examine whether the striatal nerve terminals have more severe destruction than nigral dopaminergic cell itself in the MPTP-treated mosue model of Parkinson's disease, the striatal dopamine and dopamine transporter were measured by HPLC and quantitative immunoblotting, respectively. The number of nigral dopaminergic cell was counted by immunohistochemical staining for tyrosine hydroxylase.
The degree of reduction in the level of striatal dopamine, in the level of striatal dopamine transporter and in the number of nigral dopaminergic cell correlated well. The degree of reduction in the level of striatal dopamine and striatal dopamine transporter was greater than the degree of reduction in the number of nigral dopaminergic cell.
This study shows that damage of the nerve cell body the substantia nigra is less severe than that of the nerve terminal in the striatum, which allows an opportunity for neuroprotective or halting therapeutic modalities in Parkinson's disease.
Key Words : Parkinson's disease, MPTP, mouse, dopaminergic cell,
dopamine transporter, western blot
Student Number : 91801-886
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