@article{oai:tmdu.repo.nii.ac.jp:00000473,
 author = {Ying-Lan, SHEN and Keiji, HIRAI and Yoshifumi, KATAYAMA and Ying-Lan, SHEN and Keiji, HIRAI and Yoshifumi, KATAYAMA},
 issue = {1},
 journal = {The bulletin of Tokyo Medical and Dental University},
 month = {Mar},
 note = {Intracellular recordings were made from bullfrog sympathetic ganglion cells to elucidate effects of 2-n-butyl-1-(4-methylpiperazinyl)-5,6-methylenedioxyindene・2HCI (TN-871) on synaptic transmission. TN-871 at 30 nM augmented cholinergic nicotinic fast excitatory postsynaptic potentials (fast EPSPs), whereas the drug at 3 µM reversibly depressed them, without affecting acetylcholine induced depolarizations. TN-871 did not affect active and passive electrical properties of the ganglion cells. The quantal analysis method was applied to the fast EPSPs in a 0.54 mM Ca2+/7.56 mM Mg2+ Ringer’s solution. The mean quantal content was significantly increased by TN-871 at 30 nM but significantly at 3 µM. TN-871 at 300 nM either increased or decreased the mean quantal content. The mean quanta! size of the fast EPSPs was not changed by TN-871 at the concentrations examined. Fast EPSPs in a 0.99 mM Ca2+/4.86 mM Mg2+ Ringer’s solution were not decreased affected by nicardipine, but were inhibited in amplitude by w-conotoxin in a concentration­ dependent manner. It is likely that TN-871, in high concentrations, might block w-conotoxin­ sensitive N-type calcium channels in the presynaptic terminals. These results indicate that TN-871 modulates transmitter release from preganglionic nerve terminals without changing the postsynaptic sensitivity of the ganglion cells to ACh.},
 pages = {19--29},
 volume = {42},
 year = {1995}
}