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Molecular and Cellular Biochemistry • 2004 | View Paper
“The specific nicotinic antagonists hexamethonium bromide (100 microM), dihydro-beta-erythroidine (50 microM), mecamylamine (50 microM), and tubocurarine (50 microM) blocked the responses to nicotinic agonists.”
“The nicotinic antagonists d-tubocurarine and dihydro-beta-erythroidine (DH beta E, both 10 microM) reversibly reduced the reliability of the spike firing during swimming and reduced the amplitude of the on-cycle EPSP by 16%.”
“The nicotinic antagonists mecamylamine and d-tubocurarine (both 5 microM) reduced the duration of episodes of fictive swimming recorded from the ventral roots, in spinal embryos.”
“The nicotinic response was antagonized by dihydro‐beta‐erythroidine, d‐tubocurarine and mecamylamine (10‐20 microM) but not by alpha‐bungarotoxin (10 microM).”
“Additions of the nicotinic antagonists hexamethonium and D-tubocurarine to the bathing solution reversibly attenuated the ACh-induced depolarization, while the muscarinic antagonist atropine did not have any effect.”
“Nicotinic cholinergic blocker, d-tubocurarine , inhibited to a greater extent responses to nicotinic cholinomimetics, while atropine, muscarinic cholinergic blocker, inhibited responses to muscarinic cholinomimetics.”
Neirofiziologiia = Neurophysiology • 1988 | View Paper
“This effect of MCC to increase ACh release from rat hippocampus and frontal cortex was antagonized by the nicotinic antagonists dihydro‐β‐erythroidine and d‐tubocurarine , but not by α‐bungarotoxin or by the muscarinic antagonist atropine.”
“The presence of nicotinic presynaptic receptors blocked by tubocurarine , and muscarinic presynaptic receptors blocked by atropine, which regulate synaptic transmission by facilitating and depressing the ACh release respectively, is discussed.”
“This increase of Li+ uptake by Carb was inhibited by d-tubocurarine , an antagonist of nicotinic AChR. Thus, a new method was established for detection of the activity of nicotinic AChR synthesized in oocytes injected with exogenous mRNA.”
“Their primary mode of action appears to be as agonists at the level of the acetylcholine receptor, a view supported by the observation that their effects may be blocked by the nicotinic antagonists d-tubocurarine and gallamine.”