Evidence for M₂ and M₃ Muscarinic Receptor Involvement in Cholinergic Excitatory Junction Potentials Through Synergistic Activation of Cation Channels in the Longitudinal Muscle of Mouse Ileum

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  • Matsuyama Hayato
    Laboratory of Pharmacology, Department of Veterinary Medicine, Faculty of Applied Biological Science, Gifu University, Japan
  • Tanahashi Yasuyuki
    Laboratory of Pharmacology, Department of Animal Medical Sciences, Faculty of Life Sciences, Kyoto Sangyo University, Japan
  • Kitazawa Takio
    Department of Pharmacology, School of Veterinary Medicine, Rakuno Gakuen University, Japan
  • Yamada Masahisa
    Common Resources Group, Okinawa Institute of Science and Technology, Japan
  • Komori Seiichi
    Laboratory of Pharmacology, Department of Veterinary Medicine, Faculty of Applied Biological Science, Gifu University, Japan
  • Unno Toshihiro
    Laboratory of Pharmacology, Department of Veterinary Medicine, Faculty of Applied Biological Science, Gifu University, Japan

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タイトル別名
  • Evidence for M<sub>2</sub> and M<sub>3</sub> Muscarinic Receptor Involvement in Cholinergic Excitatory Junction Potentials Through Synergistic Activation of Cation Channels in the Longitudinal Muscle of Mouse Ileum

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Cholinergic nerve–mediated excitatory junction potentials (EJPs) in the longitudinal muscle of mouse ileum were characterized by using M2 or M3 muscarinic receptor–knockout (KO) mice and 1-[β-[3-(4-methoxyphenyl) propoxy]-4-methoxyphenethyl]-1H-imidazole hydrochloride (SK&F 96365) and pertussis toxin (PTX). EJPs evoked by electrical field stimulation (EFS) in wild-type preparations, initially determined to be cholinergic in origin using tetrodotoxin, atropine, and eserine, were profoundly depressed after SK&F 96365 treatment known to block muscarinic receptor–operated cation channels. A similar depression of the EJPs was also observed by PTX treatment, which is predicted to disrupt M2-mediated pathways linked to cation channel activation. In M2-KO mouse preparations, cholinergic EJPs were evoked by EFS with their relative amplitude of 20% – 30% to the wild-type EJP and strongly inhibited by SK&F 96365. No cholinergic EJP was seen in M3-KO as well as M2/M3 double-KO preparations. The results suggest that the wild-type cholinergic EJP is not a simple mixture of M2 and M3 responses, but due to synergistic activation of cation channels by both M2 and M3 receptors in the murine ileal longitudinal muscle.

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