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Regulation of striatal preproenkephalin mRNA levels in MPTP‐lesioned mice treated with estradiol
Author(s) -
D'Astous Myreille,
Morissette Marc,
Callier Sophie,
Di Paolo Thérèse
Publication year - 2005
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.20412
Subject(s) - mptp , neuroprotection , striatum , dopamine , endocrinology , medicine , chemistry , monoamine neurotransmitter , messenger rna , enkephalin , pharmacology , biology , serotonin , receptor , biochemistry , dopaminergic , opioid , gene
We reported previously the protective effect of 17β‐estradiol (17β‐E 2 ) on 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐induced dopamine (DA) depletion. This protection was stereospecific, because 17β‐E 2 showed activity but 17α‐estradiol (17α‐E 2 ) did not. The mechanisms by which estradiol exerts its beneficial effects, however, remain unknown. We investigated a possible implication of enkephalins (ENK) in neuroprotective activity of 17β‐E 2 . Protection against MPTP‐induced DA depletion was obtained with 17β‐E 2 but not 17α‐E 2 . MPTP lesion increased striatal preproenkephalin (PPE) mRNA levels and they remained elevated in 17α‐E 2 ‐treated MPTP mice whereas 17β‐E 2 treatment decreased these levels to control values. This is the first report of estradiol modulation of striatal PPE mRNA in mice. Negative and significant correlations between DA levels, vesicular monoamine transporter (VMAT 2 ) density, and PPE mRNA were observed in the striatum of lesioned animals. This effect of 17β‐E 2 on PPE mRNA after a lesion could be one of many mechanisms by which this steroid exerts its neuroprotective activity. © 2005 Wiley‐Liss, Inc.