神経型ニコチン性アセチルコリン受容体のCa<SUP>2+</SUP>を介した脱感作機能の解明

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タイトル別名
  • Desensitizing Function of Calcium Mobilized by the Postsynaptic Neuronal-Type Nicotinic Acetylcholine Receptors at the Neuromuscular Junction
  • 神経型ニコチン性ァセチルコリン受容体のCa2+を介した脱感作機能の解明
  • シンケイガタ ニコチンセイ ァセチルコリン ジュヨウタイ ノ Ca2 オ カイシタ ダッカンサ キノウ ノ カイメイ

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Neuronal-type nicotinic acetylcholine receptors (N-nAChR) are co-localized with muscle-type (M-)nAChR in the postjunctional endplate membrane of adult skeletal muscle fibers. The postsynaptic desensitizing functions of the N-nAChR at the neuromuscular junction and at single skeletal muscle cells have been investigated using aequorin luminescence and fluorescence confocal imaging. A biphasic elevation of local intracellular Ca2+ is elicited by prolonged nicotinic action at the mouse muscle endplates. The contractile fast and noncontractile slow Ca2+ components are operated by postsynaptic M- and colocalized N-type nAChR, respectively. We have named the latter slow one RAMIC (receptor-activity modulating intracellular Ca2+). The N-nAChR are activated by nicotine and choline, and RAMIC are antagonized by methyllycaconitine and dihydro-β-erythroidine. Neuromuscular functions may be regulated by a dual nAChR system to maintain the normal postsynaptic excitability. Certain N-nAChR may be also endowed with the same functional role in the central nervous system.

収録刊行物

  • 薬学雑誌

    薬学雑誌 119 (1), 1-15, 1999

    公益社団法人 日本薬学会

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