Rat Parotid Gland Research Articles

Effects of Exogenous Thyroid Hormone on the Postnatal Morphogenesis of the Rat Parotid Gland

Administration of thyroid hormone has been shown to accelerate the early postnatal development of the rat parotid gland, but these studies have dwelt almost entirely on biochemical changes. The objective of this study was to describe the effects of exogenous thyroid hormone on morphologic aspects of the developing parotid gland, in particular the transient appearance of scattered mucous cells in this otherwise serous gland. Pups were given a daily subcutaneous injection of thyroxine (T(4)) of 0.1, 0.5, or 5.0 microg/g body weight, vehicle only (injection control), or no injection (normal control) beginning at 4 days, and killed for the collection of blood and parotid glands at intervals through 15 days. The serum was analyzed for T(4) and the glands were examined by light and electron microscopy. The results indicated that both serum T(4) and the pace of gland development were proportional to the dose of T(4). In particular, T(4) accelerated decreases in acinar size and gland area occupied by stroma and translocation of a subset of cells with small secretory granules, deeply stained with periodic acid-Schiff, from acini to intercalated ducts. However, the chronology of mucous cell disappearance was indifferent to treatment. In addition, signs of toxicity, including slower gain in body weight and greatly increased apoptosis and vacuoles in the glands, occurred with the higher doses of T(4).

Optimum dose range for the amelioration of long term radiation-induced hyposalivation using prophylactic pilocarpine treatment

Background To determine dose and time dependency of pilocarpine pre-treatment protection from late damage after unilateral irradiation of the rat parotid gland. Methods and materials The right parotid gland of saline (1 mg/ml) or pilocarpine (4 mg/kg) pre-treated rats was irradiated with 10, 15 and 20 Gy. Saliva was collected from the irradiated and shielded parotid before, 30, 60, 120 and 240 days after irradiation. The number of acinar cells/gland was determined 30, 120 and 240 days after irradiation by histological examination. Results Pilocarpine pre-treated rats, protection of parotid gland function was seen in the early-intermediate phase (0–120 days) after 15 Gy and in the late phase (>120 days) after 10 and 15 Gy. Although no protection was observed after 20 Gy, a stimulatory effect of pilocarpine on the non-irradiated gland resulted in a significant increase in total saliva secretion. The increase in function after pilocarpine treatment was paralleled by a significant increase in the number of acinar cells in both the irradiated and shielded glands. Conclusions Pre-irradiation treatment with pilocarpine induces compensatory response, at lower doses, in the irradiated and at higher doses in the non-irradiated gland reducing late damage, due to stimulation of unirradiated or surviving cells to divide.

The peptidergic innervation of the rat parotid gland: Effects of section of the auriculo-temporal nerve and/or of otic ganglionectomy

The origin/pathways of peptidergic nerves contributing to the parotid gland contents of vasoactive intestinal peptide (VIP), substance P and calcitonin gene-related peptide (CGRP) were investigated by performing surgery on one side of the rat. Comparisons (based on total amount of peptide) were made between the gland on the operated side and the contralateral gland 7 days postoperatively. Otic ganglionectomy showed that almost all of the parotid gland contents of VIP (98%) and substance P (98%) were due to the otic connection, while this was true for only a minor portion (32%) of the CGRP-gland content. Section of the auriculo-temporal nerve showed that almost all of the VIP- and substance P-containing nerve fibres reached the parotid gland via this nerve, as judged by a reduction in the VIP-content by 88% and in the substance P-content by 93%, while the CGRP-content was only reduced by 37%. Section of the auriculo-temporal nerve combined with otic ganglionectomy did not reduce the gland contents of CGRP and substance P further than just otic ganglionectomy. Thus, the auriculo-temporal nerve is not likely to innervate the parotid gland with CGRP- and/or substance P-containing nerve fibres from the trigeminal ganglion.

Parasympathetic non-adrenergic, non-cholinergic transmission in rat parotid glands: Effects of cholecystokinin-A and -B receptor antagonists on the secretory response

Recent studies show I.V. administered pentagastrin and cholecystokinin to evoke protein/amylase secretion from the rat parotid gland and to stimulate gland protein synthesis, the two phenomena being abolished by cholecystokinin receptor antagonists. In the rat parotid gland, non-adrenergic, non-cholinergic transmission mechanisms contribute to secretion of fluid and protein/amylase. Since cholecystokinin may act as a neurotransmitter, activation of cholecystokinin receptors of the gland might contribute to the parasympathetic nerve-evoked secretion. In this study, the parasympathetic innervation was stimulated in non-atropinized (in periods of 2 min) or atropinized (in periods of 3 min) pentobarbitone-anaesthetized rats before and after administration of the cholecystokinin-A receptor antagonist lorglumide (48 mg/kg, I.V.) and the cholecystokinin-B receptor antagonist itriglumide (5.5 mg/kg, I.V.). The non-adrenergic, non-cholinergic transmission fatigues rapidly resulting in declining responses. Therefore, atropinized rats, not receiving the cholecystokinin receptor antagonists, had to serve as controls. Neither at a stimulation frequency of 10 Hz nor of 40 Hz were the secretory responses of the atropinized rats affected by the receptor antagonists. After lorglumide, the saliva volume and the amylase output were (expressed as percentage of the response to the stimulation period before the administration of the antagonist) 98.0 ± 3.8% ( vs. control 91.1 ± 4.0%) and 91.9 ± 4.9% ( vs. 87.7 ± 3.7%) at 10 Hz, respectively, and 79.8 ± 4.5% ( vs. 77.3 ± 2.1%) and 73.6 ± 5.3% ( vs. 71.7 ± 2.3%) at 40 Hz, respectively. After itriglumide, the corresponding percentage figures for saliva volume and amylase output were, at 10 Hz, 99.5 ± 8.9% ( vs. 92.0 ± 2.8%) and 95.8 ± 11.8% ( vs. 89.2 ± 6.4%), respectively, and, at 40 Hz, 74.0 ± 3.1% ( vs. 79.6 ± 2.2%) and 66.6 ± 3.3% ( vs. 63.9 ± 6.0%), respectively. Similarly, the antagonists were without effect on the parotid secretory responses of non-atropinized rats subjected to stimulation at 10 Hz. Thus, under physiological conditions, the cholecystokinin receptors of the parotid gland are likely to be stimulated by circulating hormones rather than by nervous activity.

Expression of muscarinic receptor subtypes in salivary glands of rats, sheep and man

In rat parotid, submandibular and sublingual glands and in ovine parotid and in human labial glands, the expression of muscarinic receptor subtypes was examined by immunoblotting and immunohistochemistry. Functional correlates were searched for in rat salivary glands. In the rat submandibular and sublingual glandular tissues clear signals of muscarinic M1 and M5 receptors could be detected in the immunoblotting and vague bands for muscarinic M3 and, in particular for, M4 receptors. The rat parotid gland differed. In this gland, the signal was less obvious for the muscarinic M1 receptor, and further, muscarinic M4 receptors appeared more strongly marked than in the submandibular glands. The results from the immunohistochemistry could be interpreted as the muscarinic M4 receptors are located on nerve fibres, since the outer layer of lobuli were densely stained. Intraglandular vessels in the rat submandibular and parotid glands showed expression of M3 receptors. In contrast to the parotid gland, the submandibular vessels also expressed M1 and M2 receptors. Occasionally M5 receptors appeared in the arteries and veins also. The functional studies in the rat confirmed muscarinic M1 receptor mediated secretion in the submandibular gland. Since the M1 receptor blockade did not affect submandibular blood flow, indirect vascular effects could not in total explain the secretory inhibition. Also in the human labial glands, muscarinic M1, M3 and M5 receptors occurred. No or low amounts of muscarinic M2 and M4 receptors could be detected. In patients with Sjögren-like symptoms an up-regulation of M3, M4 and M5 receptors was apparent in the labial glands. In ovine parotid glands all receptors could be detected, but constantly with vague bands for muscarinic M2 receptors. In conclusion, muscarinic M1 receptors seem to be expressed in seromucous/mucous glands. A secretory effect by muscarinic M5 receptors is not to be excluded, since they were expressed in all the glands examined. However, other functions, such as promotion of inflammation, cell growth and proliferation are possible as well.

Evidence for amylase release by cGMP via cAMP-dependent protein kinase in rat parotid acinar cells

Amylase release from the rat parotid gland is primarily mediated by a cAMP-dependent protein kinase (PKA). We previously reported that cGMP/cGMP-dependent protein kinase (PKG) signaling evokes amylase release. In the present study, we investigated whether cGMP-mediated amylase release might be due to cGMP/PKA signaling, as well as cGMP/PKG pathway. Activation of PKA by cGMP was required 100–1000-fold greater concentration than activation by cAMP in a parotid cytosol fraction. Synergistic activation of PKA by the combination of physiological cAMP and low concentration of cGMP was observed. Amylase release from intact acinar cells was synergistically stimulated by the combination of diBu-cAMP and 8-pCPT-cGMP. cGMP dose-dependently stimulated amylase release from saponin-permeabilized parotid acinar cells. Phosphorylation by cGMP produced phosphorylated proteins of the same size as those produced by cAMP. Phosphorylation by cGMP was inhibited by the addition of PKA inhibitor, H-89. These results suggest that cGMP activates both PKG and PKA. Thus, it appears that both cGMP/PKG and cGMP/PKA pathways mediate amylase release from rat parotid acinar cells.

Chronic hyperglycaemia increases TGFβ2 signaling and the expression of extracellular matrix proteins in the rat parotid gland

The majority of the oral manifestations of diabetes mellitus are secondary to a reduced salivary flow, whose causes are still poorly understood. In the kidney, diabetes complications involve increased Transforming Growth Factor β (TGFβ) production and the thickening of basement membrane in small vessels. By using immunohistochemistry and western blotting, we studied the expression and signaling of TGFβ and the distribution of extracellular matrix (ECM) proteins: laminin, fibronectin, collagens III, IV and V in the parotid gland of control and diabetic rats, 30 and 60 days after streptozotocin injection (D30 and D60). At D30, there was an important increase of laminin whereas fibronectin and collagen V were moderately augmented. At D60, an additional increase of all ECM proteins was observed. TGFβ1 expression was not affected at any time. In contrast, TGFβ2 levels were significantly higher at D30, concomitant with increased TGFβ receptor II (TβRII), phosphorylated Smads 2 and 3 (pSmads 2–3) and Latent TGFβ Binding Protein 1 (LTBP1). At D60, TGFβ2 and TβRII were still increased, whereas phosphorylation of Smads was markedly decreased, and LTBP1 returned to control levels. In the control groups, TGFβ2 labeling was localized preferentially in ductal cells, whereas at D30 and D60 the staining was also observed in acinar cells. The same pattern of distribution was observed for pSmads 2–3 at D30, especially in nuclei. At D60, labeling was weak and dispersed throughout the cytoplasm. These data suggest that hyperglycaemia increases the deposition of ECM proteins in the rat parotid gland, possibly through augmentation of TGFβ2 expression and signaling.

Apoptosis during the salivary gland enlargement

Aims: A close relationship between cell proliferation and subsequent apoptosis has been established in several organs and tissues. The aim of the present study was to investigate whether there is an increased apoptotic activity in the hypertrophy/hyperplasia of the rat parotid and submandibular glands induced by the β-agonist stimulation (isoproterenol, IPR) and soy feeding. In both experimental models hypertrophy and hyperplasia developed simultaneously. Material and methods: Female Wistar rats weighing 200–250g were used. The level of apoptosis was measured by the activity of caspase-3/7 (effector caspase) from the mitochondria-free supernatants of tissue homogenates using a chemiluminescent assay. Results and conclusion: Marked enlargement of the parotids were detected in both IPR-treated and soya fed animals but the same increase of submandibular gland weights were produced only by IPR. In enlarged glands the elevated level of apoptosis was demonstrated. The soy feeding failed to induce glandular enlargement and increased caspase-3/7 activity on submandibular glands. The mastication plays an important role in maintaining normal morphology and function of the salivary glands whereby increased mastication leads to hypertrophy of glands. The animals fed by raw soybean had to exert a higher chewing activity. To eliminate this effect subsequent experiment we used dry powder or powdered soy mixed with water. The data of this experiment confirmed the effect of mastication on the condition of salivary glands. At the same time our findings demonstrated that by switching off the higher masticatory activity it could not inhibit the effect of soy feeding on the parotid enlargement. In the investigated experimental models enlargement of the salivary glands and the increased level of the apoptosis seem to be coupled processes. Supported by: OTKA T-046511 and ETT-384, Hungary

Syntaxin6 separates from GM1a-rich membrane microdomain during granule maturation

Since it was reported that components of immature secretory granules (ISGs) are different from those of mature secretory granules (MSGs) in rat parotid acinar cells, we have been considering that components of secretory granules (SGs) change dynamically during granule maturation. As the first step to understand the mechanism of granule maturation, we separated low-density detergent-resistant membrane fractions (DRMs) from purified SGs of rat parotid gland. When SGs were lysed by the detergent Brij-58, syntaxin6 and VAMP4 were found in DRMs that were different from the GM1a-rich DRMs containing VAMP2. Because syntaxin6 and VAMP4 are known to be related to granule formation, we attempted to separate DRMs from ISGs. To enrich for ISGs, glands were removed from rats 5 h after intraperitoneal injection of isoproterenol and used to purify the newly synthesized granules. Compared to mature granules prepared without injection, these newly formed granules were lower in density and contained higher concentrations of syntaxin6, VAMP4, and γ-adaptin. This composition is consistent with the characterizations of ISGs. DRMs isolated from the newly formed granules were GM1a-rich and contained syntaxin6, VAMP4, and VAMP2 together. Thus, our findings suggest that syntaxin6 and VAMP4 associate with a GM1a-rich membrane microdomain during granule formation but enter a separate membrane microdomain before transport from granules during maturation.

Neural- and Hormonal-induced Protein Synthesis and Mitotic Activity in the Rat Parotid Gland and the Dependence on NO-generation

Neural- and Hormonal-induced Protein Synthesis and Mitotic Activity in the Rat Parotid Gland and the Dependence on NO-generation

TRAFFICKING AND FUNCTION OF THE EPITHELIAL SODIUM CHANNEL ARE INHIBITED BY EPIDERMAL GROWTH FACTOR IN A RAT PAROTID GLAND CELL LINE.

Background At the time of birth, the major pathway regulating lung fluid absorption is transepithelial Na+ movement via epithelial sodium channels (ENaCs). The density of ENaC proteins is high in the apical membranes of the type II alveolar cells and its expression and function are regulated by many agents, including steroids and growth factors. The rat parotid gland cell line (PAR-C5) expresses all ENaC subunit proteins (α, β, andγ), but monolayers grown in media containing EGF do not demonstrate significant ENaC function. Objective and Methods PAR-C5 cells were studied to examine the effect of EGF on ENaC function and trafficking. Cells were seeded on permeable filter supports in the presence or absence of EGF (20 ng/mL) and/or dexamethasone (0.1 μM). After the monolayers formed tight junctions as demonstrated by transepithelial resistances > 200 Ω.cm2 (mean resistance 513 Ω.cm2), permeable filters were mounted in Ussing chambers and Na+ transport was determined by the amiloride (10 μM)-sensitive component of the short-circuit current (Isc). α-ENaC protein content of similarly treated cells was examined by Western blot. α-ENaC localization in PAR-C5 cells was determined by confocal microscopy following staining with anti-α-ENaC antibody. Results The percent change in amiloride-sensitive Isc was 41.8 ± 5.0% in the absence versus 8.5 ± 5.5% in the presence of EGF (p = .0131). Dexamethasone increased the percent change in amiloride-sensitive Isc to 67.7 ± 12.1% in the absence and 60.3 ± 5.7% in the presence of EGF (p = .234). Despite differences in ENaC function, the amount of α-ENaC protein expression was similar in the presence or absence of EGF. However, PAR-C5 cells grown in the presence of EGF demonstrated less α-ENaC localization in the membrane portion compared with those cells grown in the absence of EGF. Conclusion These results suggest that EGF inhibits the intracellular trafficking of α-ENaC into the plasma membranes in the PAR-C5 cell line. Since animal in utero studies suggest that EGF supplementation may be used to reverse pulmonary hypoplasia, further investigation is needed to characterize the signaling mechanisms whereby EGF and other growth factors modulate intracellular ENaC trafficking in different cell types.

Effects of Streptozotocin‐Induced Type 1 Diabetes Mellitus on Total Protein Concentrations and Cation Contents in the Isolated Pancreas, Parotid, Submandibular, and Lacrimal Glands of Rats

This study investigated the effect of streptozotocin (STZ)-induced type 1 diabetes mellitus (DM) on total protein concentration and levels of sodium (Na+), potassium (K+), magnesium (Mg2+), zinc (Zn2+), copper (Cu2+), calcium (Ca2+), and iron (Fe2+) in the pancreas, parotid, submandibular, and lacrimal glands of the rat, compared to age-matched control animals. Protein concentrations were measured by the Bradford Assay, whereas levels of Na+, K+, Mg2+, Zn2+, Cu2+, Ca2+, and Fe2+ were measured by flame photometry and atomic absorbance spectrophotometry. The results show marked changes in the characteristics of diabetic and control animals. Diabetic rats and their different glands weighed significantly (P < 0.05) less compared to age-matched controls. Diabetic rats also have significantly elevated blood glucose and significantly reduced plasma insulin, compared to controls. The results also show that the concentrations of proteins and levels of cations were significantly (P < 0.05) reduced in the pancreas, parotid, submandibular and lacrimal glands of diabetic rats, compared to glands from age-matched animals. These differences in the cation contents and protein levels in STZ-induced DM in this study, along with supporting evidences from previous studies, may provide evidence for the development of long-term complications of DM including exocrine gland deficiencies.

Pentagastrin‐induced nitric oxide‐dependent protein secretion from the parotid gland of the anaesthetized rat

Infusion of pentagastrin (20 microg kg(-1) h(-1), i.v.) for 10 min evokes protein output but no overt fluid secretion from the parotid gland of the rat, as revealed by increased protein concentration in a subsequent wash-out flow of saliva in response to a bolus injection of methacholine (5 microg kg(-1), i.v.) 10 min later. Using this experimental set-up, the contribution of nitric oxide (NO) generation to the protein and amylase response evoked by pentagastrin was investigated. Neither the neuronal type NO synthase inhibitor N(omega)-propyl-L-arginine (N-PLA; 30 mg kg(-1), i.v.) nor the non-selective NO synthase inhibitor L-NAME (30 mg kg(-1), i.v.) as such affected the methacholine-evoked volume response or the outputs of protein and amylase. However, when preceeded by the pentagastrin infusion, the expected increases in concentrations of protein (145%) and amylase activity (127%) of the methacholine-evoked response (compared to a pre-infusion methacholine response) were reduced to 68 and 74%, respectively, in the presence of N-PLA, and to 70 and 63%, respectively, in the presence of L-NAME. Thus, NO generation resulting from the activity of the neuronal type NO synthase, most probably of parenchymal origin, plays an important role in the pentagastrin-induced protein and amylase secretion of the rat parotid gland.

Immunolocalization of E-cadherin and αE-catenin in rat parotid acinar cell under chronic stimulation of isoproterenol

E-cadherin and αE-catenin were localized in normal and chronically isoproterenol-treated acinar cells of rat parotid gland by means of immunogold labelling of Lowicryl embedded sections. Immunostaining of both experimental groups with polyclonal antibodies to E-cadherin and αE-catenin was mainly restricted to the areas of adherens junctions. Surprisingly, in isoproterenol-treated cell αE-catenin was also found on the secretory granules periphery and appeared to encircle a secretory vesicle. In isoproterenol-induced cell hyperproliferation, the maintened presence of adherens junctions components, such as E-cadherin and αE-catenin molecules, should be an essential prerequisite for tissue integrity. Our data suggest the presence of a correlation between the organization of actin and the localization of αE-catenin in the chronically isoproterenol-treated acinar cell of rat parotid gland.

Microfilaments and cellular signal transduction: Effect of cytochalasin D on the production of cAMP, inositol phosphates, and on calcium movements in rat parotid glands

Microfilaments and cellular signal transduction: Effect of cytochalasin D on the production of cAMP, inositol phosphates, and on calcium movements in rat parotid glands

Changes in the number and distribution of myoepithelial cells in the rat parotid gland during postnatal development

The mature rat parotid gland shows hardly any cell bodies of myoepithelial cells around the acini, only a few cell processes being visible. However, in the early postnatal period, the rat parotid gland shows many myoepithelial cell bodies around the acini, including the intercalated ducts. In order to clarify the reason for the disappearance of myoepithelial cells from the area around the acinus during postnatal development, changes in the number and distribution of myoepithelial cells in the rat parotid gland were examined histochemically and chronologically, with particular reference to cell proliferation and cell death. From day 7 to day 14, many myoepithelial cells showing a positive reaction with anti-actin antiserum were found around the acini and intercalated ducts, but thereafter the number of such cells decreased gradually, particularly around the acini, and had almost disappeared after day 35. BrdU/PCNA-positive myoepithelial cells surrounding the acini were easily detected on day 14, but disappeared by day 21, whereas BrdU/PCNA-positive acinar cells remained numerous even after day 21. TUNEL/ISEL staining showed no positive myoepithelial cells throughout the observation period. Transmission electron microscopy also demonstrated no myoepithelial cells with chromatin condensation characteristic of apoptosis through the observation period. These findings suggest that the main reason for the disappearance of myoepithelial cells from the area around the acinus during postnatal development is the large difference between the number of myoepithelial cells and that of acinar cells, because the acinar cells retain their proliferative activity even after myoepithelial cells have become quiescent.

Differential responses of rostral subnucleus caudalis and upper cervical dorsal horn neurons to mechanical and chemical stimulation of the parotid gland in rats

Blockage of the salivary duct can produce pain and inflammation from the build up of saliva in the parotid gland. The processing of parotid inflammation-induced pain, however, is poorly understood. The purpose of this study was to clarify the functional involvement of the trigeminal subnucleus interpolaris/caudalis transition region (Vi/Vc) and upper cervical spinal cord (C1/C2) in processing nociceptive input relevant to parotitis. The effect of capsaicin-induced parotitis was examined on a total of 37 nociceptive neurons isolated from the Vi/Vc (n = 23) and C1/C2 (n = 14) regions. Eight of 23 Vi/Vc neurons responded to mechanical distention of the parotid gland, whereas no C1/C2 neurons responded to the parotid distention. Receptive field characteristics in all neurons were examined following capsaicin injections into the parotid gland. Mechanical and cold responses increased significantly in C1/C2 but not Vi/Vc neurons following capsaicin. Receptive field sizes also increased in C1/C2 but not Vi/Vc neurons. At the Vi/Vc transition region, pinch-evoked activity increased in neurons receiving convergent inputs from the parotid gland and facial skin when compared to non-convergent neurons. The present data indicate that the hyperalgesia and referred pain associated with parotitis may result from sensitization of C1/C2, but not Vi/Vc nociceptive neurons.

Roles of Protease-Activated Receptor-2 (PAR-2), a G Protein-Coupled Receptor, in Modulation of Exocrine Gland Functions

Protease-activated receptor-2 (PAR-2), a G protein-coupled receptor, is activated by proteolytic unmasking of the N-terminal extracellular tethered ligand that presumably binds to the extracellular loop 2 of the receptor itself. PAR-2 is widely distributed in the mammalian body and plays various roles in biological events in the cardiovascular, respiratory, alimentary, and central neurons systems. PAR-2-activating peptides administered systemically to mice and rats trigger prompt salivation in vivo. In an in vitro study, PAR-2 agonists including the endogenous PAR-2 activator trypsin induce secretion of amylase and mucin from isolated rat parotid glands and sublingual glands, respectively. PAR-2-activating peptides administered systemically also modulate pancreatic exocrine secretion in vivo as well as in vitro. In the gastric mucosa, PAR-2 stimulation enhances secretion of mucus and pepsinogen and suppresses acid secretion. Tear secretion can also be caused by PAR-2-related peptides in PAR-2-dependent and -independent manners. PAR-2 thus plays a general or key role in the regulation of exocrine secretion. This review focuses on the physiologic and/or pathophysiologic roles of PAR-2 in glandular exocrine secretion. The possibility of PAR-2 as a target for drug development is also discussed.

Lipopolysaccharide induced-in vivo increases in β-defensins of the rat parotid gland

Antimicrobial beta-defensins are thought to protect epithelial surfaces. Their mobilization in response to inflammation was studied in the rat parotid gland using an ELISA assay. Bacterial lipopolysaccharide (LPS), injected into the parotid duct on one side, induced a marked local inflammatory response in the parotid gland as judged by several fold increases in myeloperoxidase activity and, in histological sections, infiltration of neutrophils. Three hours after the injection, beta-defensin 1 and 3 were increased (by 41% and 15%, respectively, P<0.01) as compared to the contralateral gland. Though still elevated 6h after the injection, the percentage figures for beta-defensin 1 were, at this time, somewhat lower (30%) compared to the situation at 3h, while those for defensin 3 were significantly higher 65% (P<0.01); neither at the early nor at the late time of observation were any changes in the level of beta-defensin 2 observed. The beta-defensins under study were not detected in submandibular and sublingual glands, neither were they detected in the inflamed submandibular gland, showing also here several fold increases in myeloperoxidase activity and, in addition, the presence of inflammatory cells, following ductal injection of LPS towards the gland.

Facial nerve section induces transient changes in sensitivity to methacholine and in acetylcholine synthesis in the rat parotid gland

Nerves exert long-term influences on the salivary glands as e.g. revealed by increases in sensitivity to secretagogues following nerve degeneration. The objective was to study the effect of unilateral facial nerve section on the sensitivity of the parotid secretory cells 2-3 weeks postoperatively, i.e. at a time when the sensitisation is thought to be fully developed. Comparisons were made between pair of glands. However, no increase in the secretory response to increasing intravenous doses of methacholine of the duct-cannulated gland on the operated side was found; neither were any decrease in the acetylcholine synthesizing capacity of the gland found. In contrast, a slight supersensitivity had developed 1 week postoperatively supporting the idea of a functional influence of the facial nerve on the secretory cells under normal conditions. Furthermore, the results combined with the previous finding of ours of decreased acetylcholine synthesis in the parotid gland 1 week after facial nerve section, suggest a rapid restitution of the nervous influence on the secretory cells between 1 and 2-3 weeks postoperatively.