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  • 1985-1989  (2)
  • Dopamine  (1)
  • Parkinson's disease  (1)
  • Cofactor kinetics
  • 1
    ISSN: 1435-1463
    Keywords: Dopamine ; micro-dialysis ; 1-methyl-4-phenylpyridinium ion ; monoamine oxidase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The acute effect of 1-methyl-4-phenylpyridinium ion (MPP+), a neurotoxin derived from 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP), was examined by the in vivo micro-dialysis technique. A dialysis cannula was implanted into rat striatum, and the changes in the concentrations of dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), and 5-hydroxyindoleacetic acid (5-HIAA) in the perfusate every 20 min after administration of MPP+ were determined by high-performance liquid chromatography with electrochemical detection (HPLC-ED). After MPP+ administration the levels of DOPAC, HVA and 5-HIAA were markedly decreased. On the contrary the level of DA was markedly increased and reached a maximum 40 min after beginning of the MPP+ administration. By postmortem analysis of the striatal tissue MPP+ was proved to cause the inhibition of monoamine oxidase (MAO), especially MAO-B. These results suggest that the acute biochemical changes induced by MPP+ in vivo were MAO inhibition and release of DA.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1435-1463
    Keywords: Parkinson's disease ; tyrosine hydroxylase ; homospecific activity ; compensatory mechanisms
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Tyrosine hydroxylase (TH) contents in the caudate nucleus, putamen, and substantia nigra from control and parkinsonism brains were measured for the first time by a sandwich enzyme immunoassay. Both the TH protein content and TH activity (Vmax) were decreased in parallel in the parkinsonian brains as compared with those of the control brains. In contrast, TH “homospecific activity” (activity per enzyme protein) was significantly increased in the parkinsonian brains. The results indicate that the decrease of TH activity in parkinsonian brains is due to the decrease of TH protein content as a result of cell death. The increase in the “homospecific activity” of residual TH in parkinsonian brain suggests such molecular changes in TH molecules as result in a compensatory increase in TH activity.
    Type of Medium: Electronic Resource
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