Non‐adrenergic, non‐cholinergic influences on parotid acinar degranulation in response to stimulation of the parasympathetic innervation in the anaesthetized rat

Ekström, Jørgen; Asztély, A.; Tobin, Gunnar

doi:10.1113/expphysiol.1996.sp003994

Cited by 14 publications

(7 citation statements)

References 16 publications

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“…Ekström 1987Ekström , 2001Ekström and Ekström 2001;Ekström et al 1993Ekström et al , 1996Ekström et al , 1998 have shown that saliva secretion may also be elicited by a variety of secretory neuropeptides housed in stromal nerve terminals. The residual stimulation still elicited in our experiments with Cloz after treatment with both muscarinic (A) and adrenergic (Phe and Pro) antagonists may be attributable to its action on receptors located on intraglandular nerve terminals causing the exocytosis of peptidic neurotransmitters in so-called non-adrenergic/noncholinergic (NANC) transmission (Ekström et al 1998).…”

Section: Discussionmentioning

confidence: 97%

Cytomorphological study on human submandibular gland following treatment with secretagogue drugs

et al. 2006

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Using specimens of human submandibular glands, we have investigated in vitro the morphological modifications induced by clozapine, a dibenzodiazepine derivative that is used in psychotic patients and that provokes hypersalivation, a side-effect of therapy. The effects of the drug, used alone or in combination with carbachol, have been compared with those observed after treatment with drugs acting on specific receptors. To quantify the response to stimulation, we have calculated (with statistical methods) the number of microvilli and microbuds (corresponding to pits seen in images obtained by transmission electron microscopy) per square micrometre of the cytoplasmic surface of the intercellular canaliculi luminal membrane in images obtained by high-resolution scanning electron microscopy. Clozapine, when directly acting on human submandibular specimens, induces a small secretory response in serous cells; this is partially decreased by muscarinic and adrenergic antagonists and by combined incubation with carbachol, thus confirming its behaviour as a partial agonist to muscarinic receptors. We also suggests that the drug acts on the nerve terminals contained within the glandular specimens.

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Section: Discussionmentioning

confidence: 97%

Cytomorphological study on human submandibular gland following treatment with secretagogue drugs

et al. 2006

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“…the co-transmitter of acetylcholine, vasoactive intestinal peptide, evoke exocytosis, demonstrating a regulatory role in this process for parasympathetic transmitters in both animals (Ekstr€ om et al 1994;Ekstr€ om & Ekstr€ om, 2001;Ekstr€ om, 2002) and humans (Del Fiacco et al 2015). In agreement with the exocytotic responses to autonomimetics, animal experiments show varying degrees of acinar granule depletion in response to the electrical stimulation of the sympathetic and parasympathetic innervations (Garrett & Thulin, 1975;Ekstr€ om et al 1994Ekstr€ om et al , 1996. Moreover, hormones, including melatonin, of particular interest in the present context, have been shown to cause the secretion of protein/amylase (C ßevik Aras & Ekstr€ om, 2008) and to evoke exocytosis in salivary glands (Loy et al 2012(Loy et al , 2015; luzindole, an MT1/MT2 antagonist with greater affinity for MT2 receptors (Radio et al 2006), abolished these secretory events evoked by melatonin.…”

Section: Discussionmentioning

confidence: 67%

Melatonin release by exocytosis in the rat parotid gland

et al. 2018

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Several beneficial effects on oral health are ascribed to melatonin. Due to its lipophilic nature, non-proteinbound circulating melatonin is usually thought to enter the saliva by passive diffusion through salivary acinar gland cells. Recently, however, using transmission electron microscopy (TEM), melatonin was found in acinar secretory granules of human salivary glands. To test the hypothesis that granular located melatonin is actively discharged into the saliva by exocytosis, i.e. contrary to the general belief, the b-adrenergic receptor agonist isoprenaline, which causes the degranulation of acinar parotid serous cells, was administered to anaesthetised rats. Sixty minutes after an intravenous bolus injection of isoprenaline (5 mg kg À1 ), the right parotid gland was removed; pre-administration, the left control gland had been removed. Samples were processed to demonstrate melatonin reactivity using the immunogold staining method. Morphometric assessment was made using TEM. Gold particles labelling melatonin appeared to be preferentially associated with secretory granules, occurring in their matrix and at membrane level but, notably, it was also associated with vesicles, mitochondria and nuclei. Twenty-six per cent of the total granular population (per 100 lm 2 per cell area) displayed melatonin labelling in the matrix; three-quarters of this fraction disappeared (P < 0.01) in response to isoprenaline, and melatonin reactivity appeared in dilated lumina. Thus, evidence is provided of an alternative route for melatonin to reach the gland lumen and the oral cavity by active release through exocytosis, a process which is under the influence of parasympathetic and sympathetic nervous activity and is the final event along the so-called regulated secretory pathway. During its stay in granules, anti-oxidant melatonin may protect their protein/peptide constituents from damage.

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“…However, the output of protein/amylase decreases markedly and the gland loses its secretory granules [1,2]. The rat parotid saliva contains hundreds of proteins/peptides as shown by high resolution 2-D electrophoresis [3].…”

Section: Introductionmentioning

confidence: 99%

RP–HPLC–ESI–MS characterization of novel peptide fragments related to rat parotid secretory protein in parasympathetic induced saliva

Ekström

Murakami

Inzitari

et al. 2009

J of Separation Science

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Two peptides (MW 1211.7 and 928.5 Da) were detected by RP-HPLC-ESI-MS analysis of parotid saliva secreted upon continuous parasympathetic stimulation. The peptide with the higher mass (PSPFr-A) corresponded to the N-terminal dodecapeptide (Fragment 1-12) of rat parotid secretory protein (PSP), while the peptide with the lower mass (PSPFr-B) corresponded to the 4-12 fragment of the same protein. During stimulation, the PSPFr-A secretion increased, while the PSPFr-B secretion decreased (HPLC-ESI-MS). In the presence of cycloheximide, PSPFr-A was not demonstrated, while the PSPFr-B secretion decreased. In the presence of aprotinin, the PSPFr-B secretion was almost abolished, while the PSPFr-A secretion increased to higher levels than those observed in the absence of the inhibitor. In vitro perfusion, with artificial solution, of stimulated rat parotid glands excluded that the fragments were derived from the circulation. Neither peptide occurred in enriched granule preparations from unstimulated glands. The results suggest that at least two pathways--granular and vesicular--are responsible for the generation of the two peptides. PSPFr-A is the first cleavage product in both pathways. PRPFr-B is probably generated from granular PSPFr-A only and, at the end of the granule mediated pathway, by the action of an enzyme of the serine protease class.

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Non‐adrenergic, non‐cholinergic influences on parotid acinar degranulation in response to stimulation of the parasympathetic innervation in the anaesthetized rat

Cited by 14 publications

References 16 publications

Cytomorphological study on human submandibular gland following treatment with secretagogue drugs

Cytomorphological study on human submandibular gland following treatment with secretagogue drugs

Melatonin release by exocytosis in the rat parotid gland

RP–HPLC–ESI–MS characterization of novel peptide fragments related to rat parotid secretory protein in parasympathetic induced saliva

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