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Tumor Necrosis Factor Modulates the Inactivation of Catecholamine Secretion in Cultured Sympathetic Neurons
Author(s) -
Soliven Betty,
Albert Julyan
Publication year - 1992
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1992.tb09364.x
Subject(s) - catecholamine , secretion , endocrinology , tumor necrosis factor alpha , medicine , sympathetic nervous system , chemistry , necrosis , norepinephrine , biology , neuroscience , dopamine , blood pressure
Cytokines exert multiple effects on cellular functions. We studied the effects of cytokines on the calcium‐dependent release of catecholamines in cultured neurons from neonatal rat superior cervical ganglia. Incubation of sympathetic neurons with recombinant human interleukin‐β (0.14‐0.7 nM) or recombinant human tumor necrosis factor‐α (1 nM) for 24‐48 h had no effect on the baseline spontaneous release and the initial K + ‐evoked [ 3 H]norepinephrine release, compared with untreated cells. A repeat K + ‐induced depolarization after 6 min resulted in a decrease of [ 3 H]norepinephrine secretion to 69 ± 5.8% (n = 11) of the initial secretion in recombinant human tumor necrosis factor treated cells, but not in control cells. The secretory response was restored when the interval between the two K + challenges was increased to 10 min. We conclude that the diminished secretory response to a repeat stimulus in recombinant human tumor necrosis factor‐treated superior cervical ganglia neurons is due to a prolonged recovery from inactivation of secretion in these cells.