@article{09fcada3d62640c090e60dc9a70e09ba,
title = "The function of presynaptic dopamine receptors on noradrenergic nerve terminals",
author = "Korczyn, {Amos D.}",
note = "Funding Information: In sympathetic nerve terminals, NA is synthetized from DA within {"}storage{"} vesicles, through the action of an enzyme, dopamine beta-hydroxylase (DBH). Sympathetic stimulation causes discharge of the contents of the vesicles, including DBH (6). DBH itself is synthetized within the cell body, and has to be delivered to the axon terminals by axonal transport. It is likely that prolonged sympathetic stimulation would deplete the terminals of NA as well as DBH. Under these conditions the rate-limiting enzyme in catecholamine formation may not be tyrosine hydroxylase but rather DBH. Prolonged sympathetic stimulation may thus cause the release of cytoplasmatic, newly synthetized DA (along with NA). The post-synaptic effecters are usually not affected by DA as they are by NA, and DA may be regarded as a false neurotransmitter under these conditions. It would be beneficial for the organism to turn off the *Supported by a grant from the Parkinson's Disease Foundation of New York City. Dr. Korczyn's present address is the Department of Physiology and Pharmacology, Sackler School of Medicine, Tel Aviv University, Ramat Aviv, Israel.",
year = "1979",
month = oct,
doi = "10.1016/0306-9877(79)90030-6",
language = "אנגלית",
volume = "5",
pages = "1131--1132",
journal = "Medical Hypotheses",
issn = "0306-9877",
publisher = "Churchill Livingstone",
number = "10",
}