Functional characterization of muscarinic receptors in rat parotid acini

Dehaye, Jean-Paul; Marino, Aída; Soukias, Y; Poloczek, Piotr; Winand, Jacques; Christophe, Jean

doi:10.1016/0014-2999(88)90539-0

Cited by 21 publications

(5 citation statements)

References 21 publications

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“…The results correlate with radioligand binding studies showing that the putative binding sites in the rat submandibular gland have a high affinity for 4-DAMP (4-diphenyl-acetoxy-N-methylpiperidine), a selective M3 antagonist (Doods et al, 1987), and with the functional studies showing that the adult rat parotid muscarinic receptor-mediated amylase release exhibit a high affinity for atropine and HHSiD (hexahydrosila-diphenidol) and a low affinity for pirenzepine (Dehaye et al, 1988). …”

Section: Discussionsupporting

confidence: 74%

Carbachol-induced Oxygen Consumption in Slices from Developing Rat Submandibular and Parotid Glands

Stojić

1998

J Dent Res

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In contrast to the submandibular gland, the developing rat parotid gland shows refractoriness to cholinergic secretagogues until 2 wks of age. To assess the underlining mechanism of this refractoriness, I investigated changes in oxygen consumption as a function of animal age in slices from rat submandibular and parotid glands, measuring both basal and carbachol-stimulated levels. The oxygen consumption was determined by a direct manometric method in the Warburg apparatus. Carbachol-induced oxygen uptake in submandibular gland slices was observed by 1 day of age and reached the adult level of stimulation by 3 wks of age. In the parotid gland, carbachol failed to stimulate oxygen uptake in the early post-natal period, and the first response was detected at 2 wks of age, reaching the adult level at 4 wks of age. Para-fluorohexahydro-sila-diphenidol (pFHHSiD), a selective M3 antagonist, inhibited carbachol-induced oxygen uptake in both glands, while pirenzepine, a selective M1 antagonist, had no effect, suggesting that the M3 muscarinic receptors are involved in this process. The respiratory effect of carbachol, in both glands, was inhibitable by ouabain and, to a lesser extent, by furosemide, indicating that carbachol-enhanced oxygen uptake is due to Na,K-ATPase and that the furosemide-sensitive co-transport of Na+ entry is underdeveloped in immature cells. The ouabain-sensitive Na,K-ATPase activity in the parotid gland increased from birth until 28 days of age. At the time of parotid gland refractoriness to carbachol, Ca2+ ionophore A23187 caused an increase of oxygen uptake only in the presence of extracellular Ca2+. In the presence of carbachol, the effect of ionophore was significantly higher than that of ionophore alone. These results raise the possibility that the refractoriness of the parotid gland to carbachol is due to the inability of carbachol to increase Ca2+ uptake rather than to the lack of distal limb, which resides on the pathway from receptor stimulation to Na,K-ATPase activation.

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Section: Discussionsupporting

confidence: 74%

Carbachol-induced Oxygen Consumption in Slices from Developing Rat Submandibular and Parotid Glands

Stojić

1998

J Dent Res

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“…Furthermore, no small [Ca 2+ ] i increase was seen in SMG cells from M 1 /M 3 double KO mice, showing that the M 1 subtype is also involved in cholinergically activated Ca 2+ signalling in SMG cells, but much stronger stimulation is required to induce Ca 2+ signalling through this subtype. The great reduction of Ca 2+ signalling in the M 3 KO SMG cells was presumably attributable to the predominance of M 3 over M 1 in mAChR populations (Dehaye et al 1988; Dai et al 1991; Watson et al 1996; Moriya et al 1999; Bockman et al 2001), since the ability of the M 1 and M 3 subtypes to produce IP 3 in response to CCh is approximately equivalent (Burford et al 1995). The M 5 subtype seems not to be involved in induction of Ca 2+ signalling.…”

Section: Discussionmentioning

confidence: 99%

“…In terms of mAChR subtype, both the M 1 and M 3 subtypes have been reported to be present in salivary glands (e.g. Maeda et al 1988; Yamamoto et al 1996; for reviews, see Baum, 1993; Caulfield, 1993; Levey, 1993), and some reports have demonstrated predominant or exclusive expression of the M 3 subtype in the major salivary glands (Dehaye et al 1988; Dai et al 1991; Watson et al 1996; Moriya et al 1999; Bockman et al 2001). However, few physiological studies have been carried out to determine the functional relevance of specific mAChR subtypes in physiological salivation.…”

mentioning

confidence: 99%

M₃ muscarinic acetylcholine receptor plays a critical role in parasympathetic control of salivation in mice

Nakamura

Matsui

Uchida

et al. 2004

The Journal of Physiology

155

105

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The M 1 and M 3 subtypes are the major muscarinic acetylcholine receptors in the salivary gland and M 3 is reported to be more abundant. However, despite initial reports of salivation abnormalities in M 3 -knockout (M 3 KO) mice, it is still unclear which subtype is functionally relevant in physiological salivation. In the present study, salivary secretory function was examined using mice lacking specific subtype(s) of muscarinic receptor.

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“…The Ki values of these selective muscarinic antagonists in human RPE implied that carbachol stimulated PPI hydrolysis through the M3 receptor. Exocrine pancreas (Iwatsuki et al, 1989) and parotid gland (Dehaye et al, 1988) contain the M3 receptor coupled to agonist-stimulated PPI hydrolysis and cellular secretion. In a similar pattern, carbachol stimulated PPI turnover by the M3 receptor in human ocular ciliary epithelial cells (Wax and Coca-Orados 1989;Honkanen et al, 1990).…”

Section: Discussionmentioning

confidence: 99%

Receptor‐Coupled Phosphoinositide Hydrolysis in Human Retinal Pigment Epithelium

Feldman

Randolph

Johnston

et al. 1991

Journal of Neurochemistry

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Carbachol and histamine stimulated phosphoinositide (PPI) hydrolysis in cultured human retinal pigment epithelium (RPE), as reflected by an accumulation of 3H-inositol phosphates in the presence of 10 mM Li+. Carbachol increased PPI hydrolysis to greater than 600% of basal with an EC50 of 60 microM; stimulation was linear up to 60 min. This activation likely occurred via the M3 muscarinic cholinergic receptor based on the IC50 values for 4-diphenylacetoxy-N-methylpiperidine methiodide (0.47 nM), pirenzepine (280 nM), and 11-[[2-[(diethylamino)methyl]-1-piperidinyl]-acetyl]-5,11- dihydro-6H-pyrido[2,3-b][1,4]benzodiazepin-6-one (1.4 microM). Carbachol-mediated PPI hydrolysis was decreased by 80% in the absence of extracellular Ca2+. Histamine stimulated PPI turnover in a linear manner by 180% with an EC50 of 20 microM by the H1 histaminergic receptor. Serotonin, glutamate, norepinephrine, and dopamine were inactive. In human RPE, the resting cytoplasmic Ca2+ concentration, as determined by fura-2 fluorescence, was 138 +/- 24 nM. On the addition of carbachol, there was a 180% increase in peak intracellular Ca2+; addition of histamine increased intracellular Ca2+ by 187%. These results suggest receptor-mediated, inositol lipid hydrolysis is coupled to intracellular Ca2+ flux in human RPE.

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Functional characterization of muscarinic receptors in rat parotid acini

Cited by 21 publications

References 21 publications

Carbachol-induced Oxygen Consumption in Slices from Developing Rat Submandibular and Parotid Glands

Carbachol-induced Oxygen Consumption in Slices from Developing Rat Submandibular and Parotid Glands

M₃ muscarinic acetylcholine receptor plays a critical role in parasympathetic control of salivation in mice

Receptor‐Coupled Phosphoinositide Hydrolysis in Human Retinal Pigment Epithelium

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Functional characterization of muscarinic receptors in rat parotid acini

Cited by 21 publications

References 21 publications

Carbachol-induced Oxygen Consumption in Slices from Developing Rat Submandibular and Parotid Glands

Carbachol-induced Oxygen Consumption in Slices from Developing Rat Submandibular and Parotid Glands

M3 muscarinic acetylcholine receptor plays a critical role in parasympathetic control of salivation in mice

Receptor‐Coupled Phosphoinositide Hydrolysis in Human Retinal Pigment Epithelium

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M₃ muscarinic acetylcholine receptor plays a critical role in parasympathetic control of salivation in mice