Postnatal expression of α-synuclein protein in the rodent substantia nigra and striatum

被引:25
作者
Jakowec, MW
Donaldson, DM
Barba, J
Petzinger, GM
机构
[1] Univ So Calif, Dept Cell & Neurobiol, Keck Sch Med, Los Angeles, CA 90033 USA
[2] Univ So Calif, Dept Neurol, Los Angeles, CA 90033 USA
关键词
Parkinson's disease; basal ganglia; immunocytochemistry; non-A beta component of amyloid; Alzheimer's disease; development;
D O I
10.1159/000048700
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
A primary goal of our research is to elucidate the mechanisms involved in neuroplasticity of the basal ganglia in both development and in response to injury. One means to this aim is through the analysis of the ontological profile of proteins in the basal ganglia and to correlate their pattern of expression with morphological development. One protein thought to be important in neuroplasticity is alpha -synuclein. The purpose of this study was to characterize and compare the pattern of expression of alpha -synuclein protein using immunocytochemistry in the substantia nigra and striatum of the rodent in early postnatal and adult life. Our results demonstrate that there is a high level of expression of alpha -synuclein protein within cell bodies of the substantia nigra pars compacta in the Ist week of postnatal life that decreases both in intensity and number of immunoreactive cells between postnatal days 7 and 14. This is in contrast to the substantia nigra pars reticulata where alpha -synuclein protein expression in the neuropil increases after postnatal day 7. In the striatum, expression in early postnatal life is distributed in a mosaic-like fashion and becomes more diffuse after postnatal day 14. Our results support the findings of others that expression of alpha -synuclein is developmentally regulated and suggest that alpha -synuclein may play an important role in establishing the function of the basal ganglia. Understanding the role of alpha -synuclein in the normal basal ganglia may provide insights into the molecular mechanisms involved in neuroplasticity in response to injury. Copyright (C) 2001 S. Karger AG, Basel.
引用
收藏
页码:91 / 99
页数:9
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