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Neurotransmitters, Gliotransmitters, and Modulators

開催日 2014/9/11
時間 16:00 - 17:00
会場 Poster / Exhibition(Event Hall B)

Substance P regulates TRP-like nonselective cation channels and K+ channels via phosphatidylcholine-specific phospholipase C-dependent and -independent signaling pathways in nNOS-expressing GABAergic neuro

  • P1-018
  • 遠藤 利朗 / Toshiaki Endo:1 柳川 右千夫 / Yuchio Yanagawa:2 小松 由紀夫 / Yukio Komatsu:1 
  • 1:名古屋大学 / Research Institute of Environmental Medicine, Nagoya University 2:群馬大学医学系研究科 脳神経発達統御学講座 遺伝発達行動学分野 / Dept Genetic and Behavioral Neuroscience, Gunma University Graduate School of Medicine and JST, CREST,Gunma, JAPAN 

Type I neuronal nitric oxide synthase (nNOS) neurons in neocortex are a subgroup of GABAergic neurons expressing both nNOS and substance P (SP) receptors (neurokinin 1, NK1 receptors). In the present study, we investigated the actions of SP on these neurons in acute slice preparations of visual cortex obtained from GAD67-GFP knock-in mice. Whole-cell patch clamp recording and Ca2+ imaging from type I nNOS neurons revealed that SP induced a Ca2+-permeable nonselective cation current. The SP-induced current was suppressed by ruthenium red, an inhibitor of transient receptor potential (TRP) channels. To clarify the signaling pathways following the activation of NK1 receptors, we examined the effects of inhibitors of intracellular signaling molecules. Among them, D609, an inhibitor of phosphatidylcholine-specific phospholipase C (PC-PLC), induced an outward current, and additional applications of SP induced an inward current which apparently reversed the D609-induced current. Both of these responses were not observed when Cs+-based intracellular solution was used, suggesting that they were mediated by K+ channels. In this recording condition, SP induced the TRP-like current which was markedly suppressed by D609. The present results suggest that SP activates TRP-like cation channels in type I nNOS neurons via a PC-PLC-dependent signaling, and inactivates some K+ channels which are usually inhibited by a PC-PLC-dependent mechanism.

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