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

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)1189-1198
Number of pages10
JournalJournal of Neurochemistry
Volume70
Issue number3
Publication statusPublished - 1998 Mar 1

Fingerprint

Arecoline
Carbachol
Phosphatidylinositols
Rats
Brain
Cholinergic Agents
Ligands
Inositol

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Cellular and Molecular Neuroscience

Cite this

Lee, Horng Mo ; Tsai, Kuen-Jer ; Lin, Chien Huang ; Huang, Chung Lin ; Tung, Che Se. / Arecoline desensitizes carbachol-stimulated phosphatidylinositol breakdown in rat brain cortices. In: Journal of Neurochemistry. 1998 ; Vol. 70, No. 3. pp. 1189-1198.
@article{e2eb2d7a3b45449b875fd3b785583ff3,
title = "Arecoline desensitizes carbachol-stimulated phosphatidylinositol breakdown in rat brain cortices",
abstract = "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.",
author = "Lee, {Horng Mo} and Kuen-Jer Tsai and Lin, {Chien Huang} and Huang, {Chung Lin} and Tung, {Che Se}",
year = "1998",
month = "3",
day = "1",
language = "English",
volume = "70",
pages = "1189--1198",
journal = "Journal of Neurochemistry",
issn = "0022-3042",
publisher = "Wiley-Blackwell",
number = "3",

}

Arecoline desensitizes carbachol-stimulated phosphatidylinositol breakdown in rat brain cortices. / Lee, Horng Mo; Tsai, Kuen-Jer; Lin, Chien Huang; Huang, Chung Lin; Tung, Che Se.

In: Journal of Neurochemistry, Vol. 70, No. 3, 01.03.1998, p. 1189-1198.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Arecoline desensitizes carbachol-stimulated phosphatidylinositol breakdown in rat brain cortices

AU - Lee, Horng Mo

AU - Tsai, Kuen-Jer

AU - Lin, Chien Huang

AU - Huang, Chung Lin

AU - Tung, Che Se

PY - 1998/3/1

Y1 - 1998/3/1

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=0031892782&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031892782&partnerID=8YFLogxK

M3 - Article

VL - 70

SP - 1189

EP - 1198

JO - Journal of Neurochemistry

JF - Journal of Neurochemistry

SN - 0022-3042

IS - 3

ER -