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- W1990276857 abstract "If the primary mechanism by which nerve growth factor (NGF) gains access to the cell body is a specific uptake and retrograde transport from the periphery, then an inhibitor of axoplasmic transport would be expected to produce cell death. Such an inhibitor was administered to neonatal and adult rats and hamsters. A single injection of vinblastine (0.25–0.5 mg/kg s.c.) to 2-day-old rats produced massive cell death in the superior cervical ganglia (SCG). The levels of tyrosine hydroxylase in the SCG were reduced 80% at doses of 0.4 mg/kg, a dose which was uniformly fatal. Doses of 0.25 mg/kg at two days of age resulted in a 50% mortality rate and the survivors showed a permanent, partial sympathectomy. The adrenal medulla and sensory neurons did not appear to be affected. Administration of a single injection of vinblastine at maximally tolerated doses did not destroy sympathetic neurons in animals 14 days of age or older. Chronic administration of vinblastine (0.5 mg/kg every other day for two weeks) to adult rats did not destroy sympathetic neurons. Similar results were obtained in hamsters. Concomitant administration of NGF appeared to completely prevent the cytotoxic effects of vinblastine assessed by both morphological and enzymatic criteria. Several explanations are discussed which might explain these results. The similarities in the effects of vinblastine, other drugs, and axonal crush on sympathetic neurons are noted. It is proposed that all drugs which destroy sympathetic neurons (guanethidine, 6-hydroxydopamine, vinblastine) as well as anti-NGF and axonal ligation destroy the neurons by depriving the cell body of NGF from the periphery." @default.
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- W1990276857 date "1978-02-01" @default.
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- W1990276857 title "Destruction of the sympathetic nervous system in neonatal rats and hamsters by vinblastine: prevention by concomitant administration of nerve growth factor" @default.
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- W1990276857 doi "https://doi.org/10.1016/0006-8993(78)90620-0" @default.
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