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  • Keywords: L-DOPA, Parkinson's disease, dopamine, MPTP, aromatic L-amino acid decarboxylase, nigrostriatal neurons, dopamine D1 receptor antagonists.  (1)
  • Norepinephrine  (1)
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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neural transmission 107 (2000), S. 429-443 
    ISSN: 1435-1463
    Keywords: Keywords: L-DOPA, Parkinson's disease, dopamine, MPTP, aromatic L-amino acid decarboxylase, nigrostriatal neurons, dopamine D1 receptor antagonists.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary. Exogenous L-DOPA enhances dopamine metabolism in the intact and denervated striatum, and is the treatment of choice for Parkinsonism. Aromatic L-amino acid decarboxylase (AAAD) converts L-DOPA to dopamine. Blockade of dopamine D1-like receptors increases the activity of AAAD in both intact and denervated striatum. A single dose of SCH 23390, a dopamine D1-like receptor antagonist, increases the activity of AAAD in the striatum and midbrain and induces small changes in dopamine metabolism. When L-DOPA is administered after SCH 23390, there is a significant increase in the formation of 3,4-dihydroxyphenylacetic acid and dopamine turnover in striatum and midbrain compared to L-DOPA alone, suggesting further enhancement of dopamine metabolism. When the studies are repeated in the MPTP mouse model of Parkinson's disease, there is significantly more dopamine metabolism in the striatum of lesioned mice pretreated with SCH 23390 than in a comparison group treated with L-DOPA alone. These studies suggest that it may be possible to enhance the conversion of L-DOPA to dopamine in Parkinson's disease patients by administering substances that augment brain AAAD.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-2072
    Keywords: Lithium ; Norepinephrine ; Kinetics ; Brain Chemistry ; Manic-Depressive Psychoses
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of Li+ on NE turnover rates in rat heart and brain was studied. Turnover rates were determined in brain and heart by blocking tyrosine hydroxylase with L-α-methyltyrosine and following the decline of NE with time or in heart by injecting3H-NE and following the decline of NE specific activity with time. Subacute treatment with LiCl in doses that maintained a serum lithium level within the clinically therapeutic range caused: 1. A 95% increase in brain NE turnover rate without altering the steady-state level of the amine. 2. A slight but not significant increase in heart NE turnover. 3. The selective increase in brain NE turnover, compared to heart, may be attributed to the higher tissue levels of Li+ found in the brain under the conditions of study.
    Type of Medium: Electronic Resource
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