Abstract
We studied the release of [3H]norepinephrine from chicken sympathetic neurons in culture evoked by nicotinic and electrical stimulation with an intention to establish functional identity or nonidentity of the two stimuli in investigations of neurotransmitter release. Nicotinic stimulation evoked extracellular calcium dependent release of [3H]norepinephrine and the rise of intracellular calcium concentration. The release was completely blocked by nicotinic antagonists hexamethonium (100 mumol/l) and mecamylamine (10 mumol/l), and decreased by tetrodotoxin (0.3 mumol/l) and omega-conotoxin (0.1 mumol/l) to 17% and 27%, resp. The intracellular calcium response was decreased by nicotinic antagonists and tetrodotoxin, but not changed by omega-conotoxin. The electrical stimulation-evoked release was blocked by both tetrodotoxin and omega-conotoxin, and decreased by previous electrical, but not nicotinic, stimulation. The differential sensitivity to omega-conotoxin and tetrodotoxin,and the inability of nicotinic stimulation to decrease the liberation by following electrical stimulation may suggest the mobilization of different pools of the transmitter.
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