Mar 1, 1992

Tumor necrosis factor modulates the inactivation of catecholamine secretion in cultured sympathetic neurons

Journal of Neurochemistry
B Soliven, J Albert


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-1 beta (0.14-0.7 nM) or recombinant human tumor necrosis factor-alpha (1 nM) for 24-48 h had no effect on the baseline spontaneous release and the initial K(+)-evoked [3H]norepinephrine release, compared with untreated cells. A repeat K(+)-induced depolarization after 6 min resulted in a decrease of [3H]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.

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Mentioned in this Paper

Calcium [EPC]
Catecholamine Secretion
Tumor Necrosis Factor-alpha
Sympathetic Nervous System
Proteins, Recombinant DNA
Catecholamines Measurement

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