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Fasciculation and elongation protein zeta‐1 ( FEZ 1) expression in reactive astrocytes in a rat model of P arkinson's disease
Author(s) -
Sun Y.Y.,
Zhang Y.,
Sun X.P.,
Liu T.Y.,
Liu Z.H.,
Chen G.,
Xia C.L.
Publication year - 2014
Publication title -
neuropathology and applied neurobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.538
H-Index - 95
eISSN - 1365-2990
pISSN - 0305-1846
DOI - 10.1111/nan.12077
Subject(s) - substantia nigra , medial forebrain bundle , tyrosine hydroxylase , western blot , striatum , dopamine , dopaminergic , endocrinology , medicine , immunohistochemistry , parkinson's disease , forebrain , biology , chemistry , central nervous system , biochemistry , disease , gene
Aims Fasciculation and elongation protein zeta‐1 ( FEZ 1) is a critical regulator of dopaminergic neurone differentiation and dopamine release. However, to date, few studies evaluating the expression patterns of FEZ 1 in Parkinson's disease ( PD ) have been reported. The aim of this study was to investigate the expression and cellular localization of FEZ 1 in a rat model of PD and to explore the role of FEZ 1 in PD pathogenesis. Methods Male S prague– D awley rats were randomly divided into two groups: a PD group and a sham group. A model of PD was established by injecting 6‐ H ydroxydopamine H ydrobromide (6‐ OHDA ) into the right medial forebrain bundle of rats. Sham‐lesioned rats were infused with equivalent amounts of saline and served as controls. The expression levels of FEZ 1 mRNA and protein in striatum and substantia nigra were examined by real‐time polymerase chain reaction ( PCR ) and by W estern blot analysis respectively. Immunohistochemistry was performed to identify the cellular localization of FEZ 1 in sham‐lesioned and PD rats. Results W estern blot and real‐time PCR analyses demonstrated that FEZ 1 was present in normal rat brain striatum and substantia nigra. After the 6‐ OHDA injection, FEZ 1 expression gradually increased, peaked and then decreased. Immunohistochemical detection showed a shift of FEZ 1 expression from tyrosine hydroxylase positive neurones in sham‐lesioned rats to astrocytes in PD rats. Conclusions Our results indicate that FEZ 1 plays a role in the astrocytic protection of dopamine neurones and in the regulation of the neuronal microenvironment during the progression of PD .

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