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

Citation
Mw. Jakowec et al., Postnatal expression of alpha-synuclein protein in the rodent substantia nigra and striatum, DEV NEUROSC, 23(2), 2001, pp. 91-99
Citations number
44
Categorie Soggetti
Neurosciences & Behavoir
Journal title
DEVELOPMENTAL NEUROSCIENCE
ISSN journal
03785866 → ACNP
Volume
23
Issue
2
Year of publication
2001
Pages
91 - 99
Database
ISI
SICI code
0378-5866(200103/04)23:2<91:PEOAPI>2.0.ZU;2-A
Abstract
A primary goal of our research is to elucidate the mechanisms involved in n europlasticity of the basal ganglia in both development and in response to injury. One means to this aim is through the analysis of the ontological pr ofile of proteins in the basal ganglia and to correlate their pattern of ex pression with morphological development. One protein thought to be importan t in neuroplasticity is alpha -synuclein. The purpose of this study was to characterize and compare the pattern of expression of alpha -synuclein prot ein using immunocytochemistry in the substantia nigra and striatum of the r odent in early postnatal and adult life. Our results demonstrate that there is a high level of expression of alpha -synuclein protein within cell bodi es 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 increa ses after postnatal day 7. In the striatum, expression in early postnatal l ife is distributed in a mosaic-like fashion and becomes more diffuse after postnatal day 14. Our results support the findings of others that expressio n of alpha -synuclein is developmentally regulated and suggest that alpha - synuclein may play an important role in establishing the function of the ba sal ganglia. Understanding the role of alpha -synuclein in the normal basal ganglia may provide insights into the molecular mechanisms involved in neu roplasticity in response to injury. Copyright (C) 2001 S. Karger AG, Basel.