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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Journal of oral rehabilitation 30 (2003), S. 0 
    ISSN: 1365-2842
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: summary  Mastication and swallowing increase the heart rate, and posture change and respiration also modulate the heart rate. To clarify the role of mastication and swallowing in the modulation of the autonomic nervous activity, we investigated how they interact with modulation of the heart rate by changing body positions and respiration in young healthy subjects. R–R intervals of electrocardiogram at rest were significantly changed with different body positions, compared with supine and standing. A net shortening by mastication of a chewing gum base was similar in various postures. Respiration induced a periodic change in the R–R intervals, depending on the body postures, but mastication did not markedly change them in each posture. Dry swallowing at rest and spontaneous swallowing during the mastication in the sitting position induced a similar transient shortening and suppressed the respiration-induced changes after the swallowing. The net transient shortening by dry swallowing at rest was similar in the different postures. These results suggest that signals from mastication and swallowing are summated with those from body positions and respiration for shortening the R–R intervals and that signals from swallowing suppress the respiration-induced periodic changes.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 0014-4827
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Journal of oral rehabilitation 29 (2002), S. 0 
    ISSN: 1365-2842
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: summary  Mastication modulates the autonomic nervous activity of the digestive glands and the heart. The autonomic nervous balance is evaluated with spectral analysis of heart rate variability. In the present study, we investigated the effects of mastication of chewing gum base on heart rate variability to clarify the role of mastication in the sympatho-vagal balance for the regulation of the heart rate. Mastication of a chewing gum base stimulated the salivary secretion and shortened the R-R intervals in the electrocardiogram of healthy young subjects without swallowing of saliva at a fixed rate of respiration. Based on the analysis of heart rate variability, mastication increased the low-frequency band spectral power (LF), and decreased the high-frequency band spectral power (HF). The LF/HF was markedly increased by the mastication. Mastication enhances the sympathetic nervous activity and/or suppresses the parasympathetic nervous activity for the heart. Feeding behaviour with mastication might play a role in the modulation of the autonomic nervous activity.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-1424
    Keywords: Key words: Parotid — Potassium current — Chloride current — Carbachol — Isoproterenol — Calcium
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Abstract. Isoproterenol (IPR) and 8-(4-chlorophenylthio)-cyclic AMP (cpt-cAMP) enhanced carbachol (CCh)-induced fluid secretion from rat parotid glands, but had no effect by themselves. The enhancement by IPR was blocked by propranolol. In dispersed parotid acinar cells, IPR and cpt-cAMP potentiated CCh-induced K+ and Cl− currents (I K and I Cl). IPR at the concentration of 0.1 μm significantly potentiated the CCh-induced increase in intracellular Ca2+ concentration ([Ca2+] i ), but 1 mm cpt-cAMP did not. The incidence of the potentiation by IPR in CCh-induced Mn2+ entry was 31% and that by cpt-cAMP was 21%. The potentiation by IPR in the ionic currents and the [Ca2+] i was suppressed by propranolol. These results suggest that the CCh-induced fluid secretion from rat parotid glands is enhanced by IPR through the potentiation of I K and I Cl mainly by the increased cyclic AMP level and partially by the potentiated Ca2+ influx and [Ca2+] i increase, and that IPR is more effective than cpt-cAMP in the enhancement of the CCh-induced [Ca2+] i increase.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-1424
    Keywords: K+ and Cl− currents ; Tetraethylammonium ; Verapamil ; Quinine ; 4-Aminopyridine ; BK channels
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Abstract As in other salivary glands, the secretory cells of the sheep parotid have a resting K+ conductance that is dominated by BK channels, which are activated by acetylcholine (ACh) and are blocked by tetraethylammonium (TEA). Nevertheless, perfusion studies indicate that TEA does not inhibit ACh-evoked fluid secretion or K+ efflux from intact sheep parotid glands. In the present study, we have used whole-cell patch clamp techniques to show that ACh activates K+ and Cl− conductances in sheep parotid secretory cells by increasing intracellular free Ca2+, and we have compared the blocker sensitivity of the ACh-evoked whole-cell K+ current to the previously reported blocker sensitivity of the BK channels seen in these cells. The ACh-induced whole-cell K+ current was not blocked by TEA (10 mmol/l) or verapamil (100 μmol/l), both of which block the resting K+ conductance and inhibit BK channels in these cells. Quinine (1 mmol/l) and quinidine (1 mmol/l), although only weak blockers of the resting K+ conductance, inhibited the ACh-evoked current at 0 mV (K+ current), by 68% and 78%, respectively. 4-Aminopyridine (10 mmol/l) partially inhibited the ACh-induced K+ current and caused it to fluctuate. It also caused the resting membrane currents to fluctuate, possibly by altering cytosolic free Ca2+. Ba2+ (100 μmol/l), a blocker of the inwardly rectifying K+ conductance in sheep parotid cells, had no effect on the ACh-induced K+ current. We conclude that the ACh-induced K+ conductance in sheep parotid cells is pharmacologically distinct from both the outwardly rectifying (BK) K+ conductance and the inwardly rectifying K+ conductance seen in unstimulated cells. Given that in vitro perfusion and K+ efflux studies on other salivary glands in which BK channels dominate the resting conductance (e.g., the rat mandibular, rat parotid and mouse mandibular glands) have revealed an insensitivity to TEA, suggesting that BK channels do not carry the ACh-evoked K+ current, we propose that BK channels do not contribute substantially to the K+ current evoked by ACh in the secretory cells of most salivary glands.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Histochemistry and cell biology 103 (1995), S. 39-46 
    ISSN: 1432-119X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Antibodies against 21 and 27 kDa gap-junction proteins from rat liver were used to examine the identification and localization of gap-junction proteins in rat salivary glands. Acinar cells of the submandibular glands and parotid glands stained well for the 27 kDa gap junction protein and less intensely for the 21 kDa protein. Acinar cells of the sublingual glands were stained heavily for the 27 kDa gap junction protein and stained well for 21 kDa gap junction protein. No 27 kDa protein was observed in the ducts of the salivary glands. The 21 kDa gap-junction protein was distributed in some of the intercalated ducts in the parotid and submandibular glands. Immunoblotting of an extract of parotid glands with antibodies against 21 and 27 kDa gap-junction proteins revealed the presence of 21 and 27 kDa proteins in the parotid glands. It is concluded that the 27 kDa gap-junction protein in tistributed as a major component of the gap junctions in the acinar cells of all the salivary glands; the 21 kDa protein is localized as a minor component in the acinar cells and some portions of the intercalated ducts in the salivary glands. It is possible that these gap-junction proteins might contribute to the regulation of function of the salivary glands.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    European archives of oto-rhino-laryngology and head & neck 256 (1999), S. S38 
    ISSN: 1434-4726
    Keywords: Key words Taste buds ; Cytochalasin D ; Rhodamine-phalloidin ; Confocal laser microscopy ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Effects of cytochalasin D on actin filaments in cells encircling taste pores were examined to clarify the functional role of actin filaments in the maintenance of taste pores in rat fungiform papillae, using a confocal laser microscope and a scanning electron microscope. Fluorescence in the taste pore cells was detected as a ring shape produced by actin staining with rhodamine-phalloidin. Treatment of fungiform papillae with cytochalasin D diminished the positive reactions in the taste pore cells and increased the inner diameter of the ring reactions. However, deformation of the taste pores in fungiform papillae was not detected under a scanning electron microscope after treatment with cytochalasin D. These findings suggest that the organization of actin filaments encircling the taste pores contributes to regulation of the taste pore’s size in rat fungiform papillae.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 134 (1988), S. 155-160 
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Microinjection of rat brain mRNA in Xenopus oocytes induced acetylcholine, neuroteisin, serotonin, and glutamate receptors in the cells. These receptors stimulate an intracellular reaction pathway, including G-protein activation, inositol trisphosphate (IP3) formation, and Ca2+-dependent CI- channels. In the present study, we examined the roles of several protein kinases in these responses by means of inhibitors and activators of these kinases. Isoquinolinesulfonamides, inhibitors of protein kinases, caused no current responses and affected no receptor-mediated responses when injected into the oocytes at low doses (30-50 pmol), which inhibit cyclic nucleotide-dependent kinases or kinase C specifically, but abolished the receptor-mediated responses at a higher dose (300 pmol), which inhibit most protein kinases nonspecifically. Calmodulin inhibitors blocked the receptor-mediated responses strongly. Activation of cyclic nucleotide-dependent kinases or kinase C by injection of cAMP (or cGMP) or perfusion with phorbol esters caused no direct current responses but suppressed receptor-mediated responses. Current responses triggered by IP3 injection were not suppressed by these treatments. These results suggest that cAMP- (or cGMP-)dependent kinases or kinase C may not be involved in the pathway directly but may modulate it by inhibiting the initial part of the pathway (receptors, G-proteins, and/or phospholipase C), and they suggest that calmodulin may most likely be involved in the activation of Ca2+-dependent CI- channels.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
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