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Lack of α‐synuclein does not alter apoptosis of neonatal catecholaminergic neurons
Author(s) -
Stefanis Leonidas,
Wang Qiaohong,
Oo Tinmarla,
LangRollin Isabelle,
Burke Robert E.,
Dauer William T.
Publication year - 2004
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.2004.03638.x
Subject(s) - substantia nigra , pars compacta , neuroscience , catecholaminergic , biology , apoptosis , catecholaminergic cell groups , programmed cell death , parkinson's disease , microbiology and biotechnology , dopamine , medicine , dopaminergic , disease , biochemistry
α‐Synuclein is an abundant neuronal protein of uncertain function linked to Parkinson's disease. Numerous studies have proposed an antiapoptotic function for α‐synuclein, based on overexpression experiments in cell lines. To explore whether α‐synuclein has such a physiological function, we assessed the response of wild type or α‐synuclein null neonatal mouse sympathetic neurons to nerve growth factor deprivation, a well‐characterized stimulus of neuronal apoptosis. There was no difference in the rate of neuronal loss, neuronal apoptosis, or c‐jun phosphorylation. Furthermore, the absence of α‐synuclein did not alter the magnitude of naturally occurring cell death in vivo in substantia nigra pars compacta. Therefore, α‐synuclein is unlikely to play a significant role in apoptotic signalling in catecholaminergic neurons of the neonatal nervous system.