scholarly journals Serotonin and the Control of Salivation in the Blowfly Calliphora

1985 ◽  
Vol 114 (1) ◽  
pp. 307-328
Author(s):  
Barry Andrew Trimmer

The possibility that serotonin acts as a neurohormone stimulating salivation in the blowfly Calliphora vicina was studied by investigation of salivation induced by injections of high-potassium saline. Induced salivation is rapid and appears to be mediated by an active factor released into the haemolymph (High Potassium Salivary Gland Factor: HKSGF) since it is antagonized by cadmium (a calcium channel blocker) and by gramine (a serotonin-receptor blocker). The action of HKSGF on salivary glands in vitro is indistinguishable from that of serotonin: (a) it generates serotoninlike transepithelial potential changes, (b) its effect on salivation is antagonized by gramine, (c) it is as heat stable as serotonin, (d) it has the same solubility in a variety of organic solvents, (e) it is unaffected by incubation with leucine aminopeptidase or trypsin and (d) it is inactivated by rat liver monoamine oxidase type A (a serotonin deaminating enzyme). Radioenzyme assay of haemolymph from high-potassium injected flies shows that the amount of serotonin present could account for all of the retrievable bioactivity. Significant amounts of serotonin were found in the cerebral ganglion, the thoracic ganglion and nerves attached to the thoracic ganglion. Nerve sectioning experiments demonstrated that the abdominal nerves and the anterior nerves supplying the neck muscles are not involved in the normal salivatory response. However the cerebral-thoracic connective must be intact and it is suggested that release of serotonin is effected close to the main body of the thoracic ganglion. Some of the implications of the neurohormonal role of serotonin are discussed.

2020 ◽  
Vol 21 (7) ◽  
pp. 2297
Author(s):  
Dongdong Lin ◽  
Yujie Wei ◽  
Haihui Ye

Oxytocin (OT)/vasopressin (VP) signaling system is important to the regulation of metabolism, osmoregulation, social behaviours, learning, and memory, while the regulatory mechanism on ovarian development is still unclear in invertebrates. In this study, Spot/vp-like and its receptor (Spot/vpr-like) were identified in the mud crab Scylla paramamosain. Spot/vp-like transcripts were mainly expressed in the nervous tissues, midgut, gill, hepatopancreas, and ovary, while Spot/vpr-like were widespread in various tissues including the hepatopancreas, ovary, and hemocytes. In situ hybridisation revealed that Spot/vp-like mRNA was mainly detected in 6–9th clusters in the cerebral ganglion, and oocytes and follicular cells in the ovary, while Spot/vpr-like was found to localise in F-cells in the hepatopancreas and oocytes in the ovary. In vitro experiment showed that the mRNA expression level of Spvg in the hepatopancreas, Spvgr in the ovary, and 17β-estradiol (E2) content in culture medium were significantly declined with the administration of synthetic SpOT/VP-like peptide. Besides, after the injection of SpOT/VP-like peptide, it led to the significantly reduced expression of Spvg in the hepatopancreas and subduced E2 content in the haemolymph in the crabs. In brief, SpOT/VP signaling system might inhibit vitellogenesis through neuroendocrine and autocrine/paracrine modes, which may be realised by inhibiting the release of E2.


1977 ◽  
Vol 146 (3) ◽  
pp. 641-652 ◽  
Author(s):  
J Fehr ◽  
HS Jacob

To study mechanisms and mediators regulating the distribution of intravascular granulocytes between circulating and marginated pools, a human model with extreme transient margination, the neutropenia of continuous flow filtration leukophoresis, was analyzed. Studies in animals demonstrated the existence of a complement (C)-derived granulocytopenia-inducing factor. Thus, autologous plasma, exposed to nylon fibers (NF) of the filtration system, produced an acute selective decrement of circulating granulocytes and monocytes. This phenomenon was blocked by decomplementing plasma, by pretreatment of plasma with EDTA or hydrazine, and by preheating at 56 degrees C, but did occur after recombination of heat-inactivated and hydrazine-treated plasma before NF exposure. Preheating plasma at 50 degrees C did not inhibit the neutropenic response, suggesting involvement of the classical pathway of C activation. Ultrafiltration studies indicated that the NF-provoked neutropenia-inducing factor has a mol wt in the range of 10,000-30,000, and is heat stable (56 degrees C). To analyze the hypothesis that C- induced neutrophil margination might be consequent to increased cell adhesiveness to endothelial surfaces, the role of C in promoting granulocyte adherence was evaluated in vitro. Measured with a plastic Petridish assay, granulocyte adherence was significantly reduced in heat- inactivated (56 degrees C) and hydrazine-treated plasma, but adherence promoting capacity was restored by mixing the two plasmas, or by adding purified C3 to hydrazine-treated plasma. After exposure to activated C, neutrophils showed significantly increased adhesiveness which was maintained when cells were resuspended in heat-inactivated plasma, but progressively lost when resuspended in fresh plasma. On the basis of these results we conclude that granulocyte adhesiveness in vitro and margination in vivo are closely associated, C-dependent phenomena.


1994 ◽  
Vol 266 (3) ◽  
pp. L232-L237
Author(s):  
K. S. Lindeman ◽  
L. B. Fernandes ◽  
T. L. Croxton ◽  
C. A. Hirshman

To elucidate the mechanism of hypoxic relaxation of airway smooth muscle in vitro, we investigated the role of adenosine triphosphate-sensitive potassium (KATP) channels in this response. Second- and third-order porcine bronchial rings were suspended in 10-ml organ baths containing Krebs-Henseleit solution. To demonstrate the presence of KATP channels in this tissue, bronchial rings were contracted with carbachol (1 microM) in the presence of glibenclamide (100 microM), a KATP channel blocker, or the vehicle dimethyl sulfoxide (DMSO) (0.1 ml), and dose-response curves to levcromakalim (a KATP channel opener) or isoproterenol were constructed. In separate experiments, either glibenclamide or DMSO was added to the chamber and rings were contracted with carbachol (1 microM) in the presence of 95% O2-5% CO2. At the plateau, airways were relaxed with either isoproterenol (0.1 or 0.3 microM) or hypoxia (50, 28, or 0% O2, with constant 5% CO2). Glibenclamide, when compared with DMSO, shifted the dose-response curve to levcromakalim, but not to isoproterenol. Glibenclamide attenuated hypoxic relaxation in rings exposed to 50% O2 (from 35 +/- 4% to 23 +/- 3%, n = 6, P < 0.001) and increased the time to 63% relaxation in rings exposed to 50% O2 or to 28% O2. Responses in rings exposed to 0% O2 or to isoproterenol (0.1 or 0.3 microM) were not significantly altered. The ability of glibenclamide to attenuate the maximum response to 50% O2 and to increase the time to 63% relaxation during exposure to 50 or 28% O2 suggests that one component of hypoxic bronchodilation during moderate degrees of hypoxia is opening of KATP channels.


2018 ◽  
Vol 86 (7) ◽  
pp. e00183-18 ◽  
Author(s):  
D. T. Bolick ◽  
P. H. Q. S. Medeiros ◽  
S. E. Ledwaba ◽  
A. A. M. Lima ◽  
J. P. Nataro ◽  
...  

ABSTRACTEnterotoxigenicEscherichia coli(ETEC) is a major cause of traveler's diarrhea as well as of endemic diarrhea and stunting in children in developing areas. However, a small-mammal model has been badly needed to better understand and assess mechanisms, vaccines, and interventions. We report a murine model of ETEC diarrhea, weight loss, and enteropathy and investigate the role of zinc in the outcomes. ETEC strains producing heat-labile toxins (LT) and heat-stable toxins (ST) that were given to weaned C57BL/6 mice after antibiotic disruption of normal microbiota caused growth impairment, watery diarrhea, heavy stool shedding, and mild to moderate intestinal inflammation, the latter being worse with zinc deficiency. Zinc treatment promoted growth in zinc-deficient infected mice, and subinhibitory levels of zinc reduced expression of ETEC virulence genescfa1,cexE,sta2, anddegPbut not ofeltA in vitro. Zinc supplementation increased shedding and the ileal burden of wild-type (WT) ETEC but decreased shedding and the tissue burden of LT knockout (LTKO) ETEC. LTKO ETEC-infected mice had delayed disease onset and also had less inflammation by fecal myeloperoxidase (MPO) assessment. These findings provide a new murine model of ETEC infection that can help elucidate mechanisms of growth, diarrhea, and inflammatory responses as well as potential vaccines and interventions.


Blood ◽  
1997 ◽  
Vol 89 (11) ◽  
pp. 4182-4189 ◽  
Author(s):  
Robert Bortolussi ◽  
Kausalya Rajaraman ◽  
Gefei Qing ◽  
Rengaswami Rajaraman

Abstract We investigated the role of humoral factors in lipopolysaccharide (LPS) priming of polymorphonuclear leukocytes (PMN) using cells isolated from adults and from neonates. Plasma from newborn infants had decreased priming activity of adult plasma when mixed with LPS in studies measuring oxidative radical production of PMN after stimulation with a formyl bacterial oligopeptide (fMLP). This marked difference was not caused by LPS binding protein (LBP) because the LBP concentration in newborn and adult plasma were similar (138.4 ± 12.9 U for adults, and 126.9 ± 12.1 U for neonates, P = .53). Therefore, we attempted to identify other plasma factors that may contribute to LPS priming of PMN. We identified an LPS priming factor for PMN that is present in plasma, heat stable (56°C for 30 minutes), enhanced by heparin, and concentrated in cold precipitates of plasma. Because these properties resemble those of plasma fibronectin, we assessed the role of fibronectin in LPS priming of PMN. Although fibronectin in phosphate-buffered saline (PBS) had little effect on LPS priming of PMN, fibronectin in combination with other plasma factors appeared to play a role in LPS priming of PMN because (1) removing fibronectin from adult plasma dramatically decreased LPS priming activity from plasma (P < .005), (2) addition of fibronectin to fibronectin-depleted plasma restored its LPS plasma priming activity (P < .05), and (3) neutralizing fibronectin with antibody decreased the LPS priming activity of plasma (60.3 ± 1.3 v 30.2 ± 2.2, P < .01). Thus, plasma fibronectin plays a role in LPS priming of PMN in the presence of other factors in plasma.


2008 ◽  
Vol 294 (5) ◽  
pp. H2371-H2381 ◽  
Author(s):  
Gregory M. Dick ◽  
Ian N. Bratz ◽  
Léna Borbouse ◽  
Gregory A. Payne ◽  
Ü. Deniz Dincer ◽  
...  

We previously demonstrated a role for voltage-dependent K+ (KV) channels in coronary vasodilation elicited by myocardial metabolism and exogenous H2O2, as responses were attenuated by the KV channel blocker 4-aminopyridine (4-AP). Here we tested the hypothesis that KV channels participate in coronary reactive hyperemia and examined the role of KV channels in responses to nitric oxide (NO) and adenosine, two putative mediators. Reactive hyperemia (30-s occlusion) was measured in open-chest dogs before and during 4-AP treatment [intracoronary (ic), plasma concentration 0.3 mM]. 4-AP reduced baseline flow 34 ± 5% and inhibited hyperemic volume 32 ± 5%. Administration of 8-phenyltheophylline (8-PT; 0.3 mM ic or 5 mg/kg iv) or NG-nitro-l-arginine methyl ester (l-NAME; 1 mg/min ic) inhibited early and late portions of hyperemic flow, supporting roles for adenosine and NO. 4-AP further inhibited hyperemia in the presence of 8-PT or l-NAME. Adenosine-induced blood flow responses were attenuated by 4-AP (52 ± 6% block at 9 μg/min). Dilation of arterioles to adenosine was attenuated by 0.3 mM 4-AP and 1 μM correolide, a selective KV1 antagonist (76 ± 7% and 47 ± 2% block, respectively, at 1 μM). Dilation in response to sodium nitroprusside, an NO donor, was attenuated by 4-AP in vivo (41 ± 6% block at 10 μg/min) and by correolide in vitro (29 ± 4% block at 1 μM). KV current in smooth muscle cells was inhibited by 4-AP (IC50 1.1 ± 0.1 mM) and virtually eliminated by correolide. Expression of mRNA for KV1 family members was detected in coronary arteries. Our data indicate that KV channels play an important role in regulating resting coronary blood flow, determining duration of reactive hyperemia, and mediating adenosine- and NO-induced vasodilation.


1973 ◽  
Vol 12 (1) ◽  
pp. 23-35
Author(s):  
S. L. HOWELL ◽  
R.B. L. EWART

Partially purified storage granule fractions obtained from rat anterior pituitaries have been utilized to study some properties of the isolated growth hormone granules during incubation in vitro. The isolated granules showed optimal stability at room temperature in the pH range 5.5-6.5 and dissolved progressively with time at a rate which was unaffected by the presence of EDTA, EGTA, ouabain, magnesium ions, or by resuspension in hypotonic media. However, the granules were partially stabilized by the presence of calcium, tyramine or adenosine phosphates; ATP was most effective of the agents tested and induced almost complete stability. Agents known to stimulate the secretion of growth hormone from the intact cells, cyclic 3',5'-AMP, dibutyryl cyclic 3',5'-AMP, theophylline or high potassium concentrations, were each without significant effect on the isolated granules. The granule fraction was ineffective indegrading added 125I-growth hormone over a pH range of 4.5-8.5 and was unable specifically to bind exogenous 125I-growth hormone. Further experiments to elucidate a possible cytological role of nucleotides in stabilization of growth hormone during storage granule formation demonstrated that adenine nucleotides were not constituents of the isolated granules, nor were they secreted into the incubation medium concomitantly with growth hormone. Depletion of intracellular ATP levels has previously been shown to prevent the formation of growth-hormone storage granules, and it is suggested that one role of the nucleotide may be to facilitate the formation and stabilization of storage granules in the Golgi complex by interacting with the growth hormone to induce its precipitation.


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