Arecoline desensitizes carbachol-stimulated phosphatidylinositol breakdown in rat brain cortices

Horng Mo Lee, Kuen Jer Tsai, Chien Huang Lin, Chung Lin Huang, Che Se Tung

研究成果: 雜誌貢獻文章同行評審

4 引文 斯高帕斯(Scopus)


To understand the effects of arecoline administration on the muscarinic cholinergic signaling pathway, rats were injected with arecoline, 10 mg/kg i.p., and the carbachol-stimulated phosphoinositide breakdown in rat brain cortical slices was examined. In vivo administration of arecoline resulted in inhibition of carbachol-stimulated phospholnositide turnover in rat brain cortical slices. Arecoline was a partial agonist with peak effects of 30% of the maximum as obtained with carbachol. Coaddition of arecoline inhibited the carbachol-stimulated phosphoinositide breakdown. Pretreatment of rat brain cortical slices with arecoline in vitro resulted in a dose-dependent inhibition of carbachol-stimulated [3H] inositol monophosphate accumulation. The inhibition occurred rapidly, with half-maximal inhibition occurring at 15 min and maximal inhibition achieved within 60 min. The inhibition of phosphoinositide breakdown was recovered 1 h after arecoline was removed. When synaptoneurosomes were used for the ligand binding studies, arecoline pretreatment was found to have decreased the maximal ligand binding (B(max)) without inducing any marked change in binding affinity (K(D)). The influence could be recovered by incubating the synaptoneurosomes in the absence of arecoline for 2 h. Taken together, these data suggest that the underlying mechanism by which phosphoinositide turnover is inhibited is arecoline- induced receptor sequestration.
頁(從 - 到)1189-1198
期刊Journal of Neurochemistry
出版狀態已發佈 - 3月 1998

ASJC Scopus subject areas

  • 生物化學
  • 細胞與分子神經科學


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