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Science 30 April 1971:
Vol. 172. no. 3982, pp. 487 - 489
DOI: 10.1126/science.172.3982.487
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Articles

Dopamine: Stimulation-Induced Release from Central Neurons

K. Y. Ng 1, T. N. Chase 1, R. W. Colburn 1, and I. J. Kopin 1

1 Laboratory of Clinical Science, National Institute of Mental Health, Bethesda, Maryland 20014

Dopamine, synthesized in rat brain slices from labeled L-tyrosine or L-dopa, can be released by electrical stimulation of a type known to induce neuronal depolarization. Pretreatment of the animals with 6-hydroxydopamine, which destroys central catecholamine-containing nerve terminals, substantially reduced the release of dopamine synthesized from [14C]tyrosine or from a low concentration of [3H]dopa, whereas the release of dopamine formed from a high concentration of [3H]dopa remained essentially unchanged. The observations that at high concentrations L-dopa may enter noncatecholaminergic cells, undergo decarboxylation to dopamine, and subsequently be liberated in response to depolarization suggest that dopamine may act as a substitute central transmitter, possibly in serotonergic neurons. This mechanism may contribute to L-dopa's clinical effects in parkinsonian patients.


THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
Evidence for a role of the 5-HT1B receptor and its adaptor protein, p11, in L-DOPA treatment of an animal model of Parkinsonism.
X. Zhang, P. E. Andren, P. Greengard, and P. Svenningsson (2008)
PNAS 105, 2163-2168
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Levodopa-Induced Myoclonus.
H. L. Klawans, C. Goetz, and D. Bergen (1975)
Arch Neurol 32, 331-334
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Central Monoamine Metabolism in Parkinson's Disease.
T. N. Chase and L. K. Y. Ng (1972)
Arch Neurol 27, 486-491
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Science. ISSN 0036-8075 (print), 1095-9203 (online)