Miguel, JC, Abdel-Wahab, Yasser, Mathias, PCF and Flatt, Peter (2002) Muscarinic receptor subtypes mediate stimulatory and paradoxical inhibitory effects on an insulin-secreting beta cell line. BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS, 1569 (1-3). pp. 45-50. [Journal article]
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Acetylcholine (ACh), a major neurotransmitter from the autonomic nervous system, regulates the cholinergic stimulation of insulin secretion, through interactions with muscarinic receptors. The present study has characterised the individual involvement of muscarinic receptor subtypes in ACh-induced insulin secretion, using clonal P cells and selective muscarinic receptor antagonists. BRIN BD11 cells clearly expressed mRNA encoding m1-m4 whereas m5 was not detected by RT-PCR. Insulin release was measured from BRIN BD11 cells treated with ACh in the presence of muscarinic receptor antagonists at concentrations ranging from 3 nM to 1 muM. 300 nM of muscarinic toxin-3 (M4 antagonist) and 1 muM of methoctramine (M2 antagonist) increased ACh (100 muM) stimulated insulin secretion by 168% and 50% respectively (ANOVA, P<0.05). The antagonists alone had no effect on insulin secretion. In contrast, 300 nM of pirenzepine (M I antagonist) and 30 nM of hexahydro-sila-difenidol p-fluorohydrochloride (M3 antagonist) inhibited ACh stimulation by 91% and 84% respectively (ANOVA, P<0.01). It is concluded that ACh acts on different receptor subtypes producing both a stimulatory and an inhibitory action on insulin release. (C) 2002 Elsevier Science B.V. All rights reserved.
|Item Type:||Journal article|
|Faculties and Schools:||Faculty of Life and Health Sciences|
Faculty of Life and Health Sciences > School of Biomedical Sciences
|Research Institutes and Groups:||Biomedical Sciences Research Institute|
Biomedical Sciences Research Institute > Diabetes
|Deposited By:||Professor Peter Flatt|
|Deposited On:||14 Jan 2010 11:04|
|Last Modified:||09 May 2016 10:48|
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