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AIM:Toosendanin is a pre-synaptic blocker at theneuromuscular junction and its inhibitory effect is dividedinto an initial facilitative/stimulatory phase followed by aprolonged inhibitory phase.The present study investigatedwhether the subsequent inhibitory phase was due toexhaustion of the secretory machinery as a result of extensivestimulation during the initial facilitative phase.Morespecifically,this paper examined whether toosendanin coulddirectly inhibit the secretory machinery in exocrine cells.METHODS:Rat pancreatic acinar cells were isolated bycollagenase digestion.Secretion was assessed by measuringthe amount of amylase released into the extracellular mediumas a percentage of the total present in the cells beforestimulation.Cholecystokinin(CCK)-induced increases inintracellular calcium in single cells were measured with fura-2 microfluorometry.RESULTS:Effects of toosendanin on CCK-induced amylasesecretion and calcium oscillations were investigated.Toosendanin of 87-870μM had no effect on 10 pM-100 nMCCK-stimulated amylase secretion,nor did 8.7-870μMtoosendanin inhibit 5 pM CCK-induced calcium oscillations.In contrast,10 nM CCK_1 receptor antagonist FK 480 completelyblocked 5 pM CCK-induced calcium oscillations.CONCLUSION: The pre-synaptic “blocker” toosendanin is a selective activator of the voltage-dependent calcium channels, but does not interfere with the secretory machinery itself.
AIM: Toosendanin is a pre-synaptic blocker at the neuromuscular junction and its inhibitory effect is dividedinto an initial facilitative / stimulatory phase followed by a committed inhibitory phase. The present study investigating the following inhibitory phase was due tohappiness of the secretory machinery as a result of extensivestimulation during the initial facilitative phase. Specifically identified, the paper review whether toosendanin could result in the secretory machinery in exocrine cells. METHODS: Rat pancreatic acinar cells were isolated by collagenase digestion. Secretion was assessed by measuring the amount of amylase released into the extracellular mediumas a percentage of the total present in the cells beforestimulation. Cholecystokinin (CCK) -induced increases inintracellular calcium in single cells were measured with fura-2 microfluorometry .RESULTS: Effects of toosendanin on CCK-induced amylasecrecretion and calcium oscillations were investigated.Toosendanin of 87-870 μM had no effect on 10 pM-100 nMCCK-stimulated amylase secretion, nor did 8.7-870 μM toosendanin inhibit 5 pM CCK-induced calcium oscillations. In contrast, 10 nM CCK_1 receptor antagonist FK 480 completely blocked 5 pM CCK-induced calcium oscillations.CONCLUSION: The pre -synaptic “blocker ” toosendanin is a selective activator of the voltage-dependent calcium channels, but does not interfere with the secretory machinery itself.