<原著論文>ウシガエル交感神経節細胞のムスカリン性シナプス応答に対するアラキドン酸の二重作用

概要

論文の詳細を見る
The effects of arachidonic acid (AA) on the muscarinic responses in bullfrog sympathetic neurons were examined by means of the single microelectrode current- and voltage-clamp technique. Two types of muscarinic receptor-mediated responses were evoked by brief applications of ACh to the cells and termed the fast mI_<ACh> and the slow mI_<ACh> respectively, from its time couse. The fast mI_<ACh> results from the inhibition of the M-current, while the slow mI_<ACh> results from the activation of the non-M type muscarinic cation channels. In the presence of AA (20 μM), the amplitude of the fast mI_<ACh> greatly increased by about 6 times at -50 mV. Furthermore, the fast mI_<ACh> appeared at the potential level of -70 mV where the fast mI_<ACh> did not appear in the absence of AA. On the other hand, AA reduced the amplitude of the slow mI_<ACh> to about 70% at -80 mV. Neither indomethacin nor nordihydroguaiaretic acid, blockers of cyclooxygenase and lipoxygenase pathways respectively, prevented the action of AA on the muscarinic responses. These results suggest that AA not only regulates the fast mI_<ACh> but also reduces the threshold of activation of M-channels and that its metabolites do not have a major role in the augmentation of fast mI_<ACh>. On the other hand, AA inhibits the activation of non-M-type channels.
2001-03-31