Previous studies have suggested a role for the retrograde messenger, nitric oxide (NO), in methamphetamine (METH)-and 1-methyl-4-phenyl-1,2,3,6tetrahydropyridine (MPTP)-induced dopaminergic neurotoxicity. Since evidence supported the involvement of the neuronal nitric oxide synthase (nNOS) isoform i
Dopamine differentiation factors increase striatal dopaminergic function in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-lesioned mice
โ Scribed by B.K. Jin; L. Iacovitti
- Publisher
- John Wiley and Sons
- Year
- 1996
- Tongue
- English
- Weight
- 434 KB
- Volume
- 43
- Category
- Article
- ISSN
- 0360-4012
No coin nor oath required. For personal study only.
โฆ Synopsis
We have previously shown that muscle-derived difdopamine (DA) levels and a significant loss of DA cell ferentiation factors (MDF) and human recombinant bodies in the pars cornpacta of the substantia nigra are acidic fibroblast growth factor (aFGF) have beneficommon to both. Partial recovery of striatal dopaminer-cia1 behavioral and neurochemical effects on the gic function in MPTP-treated mice has been observed nigrostriatal dopaminergic neurons of 6-hydroxy-, previously following transplantation of adrenal meduldopamine (6-OHDA)-lesioned rats (Jin and Iacovitti: Neurobiol Dis 2:l-12, 1995). In the present study, we determined the effects of similar treatments on mice treated with the neurotoxin l-methyl-Cphenyl-l,2, 3,64etrahydropyridine (MPTP). Five days after unilateral striatal infusion of MDF or aFGF into MPTPlesioned mice, striatal tyrosine hydroxylase (TH) activity and dihydroxyphenylacetic acid (DOPAC) levels were bilaterally increased (20-35 %) compared to untreated (lesion only) or control (phosphate buffered saline + bovine serum albumin) mice. These increases, however, were not accompanied by change in dopamine (DA) levels, indicating an elevation of DA synthesis (THIDA) and turnover (DOPACIDA). The present findings that MDF and aFGF may have neurochemical effects in vivo on the lesioned nigrostriatal dopaminergic system suggest their potential pharmacological role in the treatment of Parkinson's disease.
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