<原著論文>ウシガエル交感神経節のニコチン性シナプス伝達に対するアラキドン酸の抑制作用

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The effects of arachidonic acid (AA) on the nicotinic responses mediated through the activation of nicotinic receptor-channel complex were examined in bullfrog sympathetic neurons. AA (20 μM) reversibly reduced the amplitude of the fast excitatory postsynaptic potentials and underlying currents evoked by preganglionic nerve stimulation in a Ca^<2+>-deficient solution. AA reduced the acetylcholine (ACh)-induced nicotinic currents (nI_<ACh>) evoked by brief applications of ACh to the cells. The dose-response curve showed the reduction of maximum response of nI_<ACh> without causing an appreciable change in the apparent dissociation constant. Indomethacin and nordihydoroguaiaretic acid, blockers of cyclooxygenase and lipoxygenase pathways respectively, did not prevent the action of AA. These results suggest that AA directly acts on the allosteric site of the nicotinic receptor-channel complex and inhibits the ion permeation through the nicotinic receptor-channels.
1998-03-31