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Changes in functioning of rat submandibular salivary gland under streptozotocin-induced diabetes are associated with alterations of Ca2+ signaling and Ca2+ transporting pumps.

https://arctichealth.org/en/permalink/ahliterature9024
Source
Biochim Biophys Acta. 2006 Mar;1762(3):294-303
Publication Type
Article
Date
Mar-2006
Author
N V Fedirko
I A Kruglikov
O V Kopach
J A Vats
P G Kostyuk
N V Voitenko
Author Affiliation
Biological Department, I.Franko Lviv National University, 4 Grushevsky St., Lviv 79005, Ukraine. fedirn01@med.nyu.edu
Source
Biochim Biophys Acta. 2006 Mar;1762(3):294-303
Date
Mar-2006
Language
English
Publication Type
Article
Keywords
Acetylcholine - analogs & derivatives - metabolism
Animals
Ca(2+)-Transporting ATPase - metabolism
Calcium - metabolism
Calcium Signaling - physiology
Cells, Cultured
Diabetes Mellitus, Experimental - complications - metabolism
Endoplasmic Reticulum - metabolism
Fluorescent Dyes - metabolism
Fura-2 - analogs & derivatives - chemistry - metabolism
Homeostasis
Inositol 1,4,5-Trisphosphate - metabolism
Ionomycin - metabolism
Ionophores - metabolism
Male
Norepinephrine - metabolism
Pancreas - cytology - metabolism
Rats
Rats, Wistar
Research Support, Non-U.S. Gov't
Saliva - chemistry - metabolism
Submandibular Gland - metabolism
Thirst
Xerostomia - etiology - metabolism
Abstract
Xerostomia and pathological thirst are troublesome complications of diabetes mellitus associated with impaired functioning of salivary glands; however, their cellular mechanisms are not yet determined. Isolated acinar cells were loaded with Ca2+ indicators fura-2/AM for measuring cytosolic Ca2+ concentration ([Ca2+]i) or mag-fura-2/AM-inside the endoplasmic reticulum (ER). We found a dramatic decrease in pilocarpine-stimulated saliva flow, protein content and amylase activity in rats after 6 weeks of diabetes vs. healthy animals. This was accompanied with rise in resting [Ca2+]i and increased potency of acetylcholine (ACh) and carbachol (CCh) but not norepinephrine (NE) to induce [Ca2+]i transients in acinar cells from diabetic animals. However, [Ca2+]i transients mediated by Ca2+ release from ER stores (induced by application of either ACh, CCh, NE, or ionomycin in Ca2+-free extracellular medium) were decreased under diabetes. Application of inositol-1,4,5-trisphosphate led to smaller Ca2+ release from ER under the diabetes. Both plasmalemma and ER Ca2+-ATPases activity was reduced and the latter showed the increased affinity to ATP under the diabetes. We conclude that the diabetes caused impairment of salivary cells functions that, on the cellular level, associates with Ca2+ overload, increased Ca2+-mobilizing ability of muscarinic but not adrenergic receptors, decreased Ca2+-ATPases activity and ER Ca2+ content.
PubMed ID
16443349 View in PubMed
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Diabetes-induced abnormalities in ER calcium mobilization in primary and secondary nociceptive neurons.

https://arctichealth.org/en/permalink/ahliterature9510
Source
Pflugers Arch. 2004 Jul;448(4):395-401
Publication Type
Article
Date
Jul-2004
Author
I. Kruglikov
O. Gryshchenko
L. Shutov
E. Kostyuk
P. Kostyuk
N. Voitenko
Author Affiliation
Bogomoletz Institute of Physiology, 4 Bogomoletz St., 01024, Kiev, Ukraine.
Source
Pflugers Arch. 2004 Jul;448(4):395-401
Date
Jul-2004
Language
English
Publication Type
Article
Keywords
Animals
Caffeine - pharmacology
Calcium - metabolism
Diabetes Mellitus, Experimental - metabolism
Diabetic Neuropathies - metabolism
Endoplasmic Reticulum - metabolism
Ganglia, Spinal - cytology - metabolism
Homeostasis - physiology
Inositol 1,4,5-Trisphosphate - metabolism
Ionomycin - pharmacology
Ionophores - pharmacology
Male
Neurons, Afferent - drug effects - metabolism
Nociceptors - drug effects - metabolism
Phosphodiesterase Inhibitors - pharmacology
Rats
Rats, Wistar
Research Support, Non-U.S. Gov't
Ryanodine Receptor Calcium Release Channel - metabolism
Abstract
Development of diabetic sensory polyneuropathy is associated with alterations in intracellular calcium homeostasis in primary and secondary nociceptive neurons. We have shown previously that in a model of streptozotocin (STZ)-induced diabetes, the calcium signal is prolonged and calcium release from ryanodine-sensitive calcium stores down-regulated in neurons of the nociceptive system. The aim of the present study was a more detailed characterization of calcium homeostasis in primary (dorsal root ganglia, DRG) and secondary (dorsal horn, DH) nociceptive neurons in STZ-induced diabetes. Fluorescence video-imaging was used to measure free cytosolic [Ca2+] ([Ca2+]i) in lumbar nociceptive neurons of control and streptozotocin-diabetic rats. Resting [Ca2+]i rose progressively in these neurons with the duration of diabetes and calcium mobilization from the endoplasmic reticulum (ER) decreased during diabetes. The amplitude of calcium release from both ryanodine- and IP3-sensitive calcium stores induced by caffeine, ionomycin, ATP or glutamate was significantly (P
PubMed ID
15048576 View in PubMed
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Endocrine regulation of the phosphatidylinositol pathway in the Norway lobster, Nephrops norvegicus, and the shore crab, Carcinus maenas.

https://arctichealth.org/en/permalink/ahliterature11161
Source
Gen Comp Endocrinol. 1996 Oct;104(1):84-91
Publication Type
Article
Date
Oct-1996
Author
R P Smullen
J A David
R M Pitman
Author Affiliation
Institute of Aquaculture, University of Stirling, Scotland.
Source
Gen Comp Endocrinol. 1996 Oct;104(1):84-91
Date
Oct-1996
Language
English
Publication Type
Article
Keywords
Animals
Binding Sites
Brachyura - metabolism
Calcium - metabolism
Cytosol - metabolism
Endocrine Glands - physiology
Inositol 1,4,5-Trisphosphate - metabolism
Intracellular Fluid - metabolism
Liver - cytology - drug effects - metabolism
Male
Muscle, Skeletal - cytology - drug effects - metabolism
Nephropidae - metabolism
Nerve Tissue Proteins - pharmacology
Pancreas - cytology - drug effects - metabolism
Phosphatidylinositols - metabolism
Radioligand Assay
Research Support, Non-U.S. Gov't
Abstract
The present study examines the mode of action of eyestalk factors, in particular crustacean hyperglycaemic hormone (CHH), on known target tissues (muscle and hepatopancreas) in two decapod crustacean species, Nephrops norvegicus and Carcinus maenas. The possibility that receptors to CHH are coupled to an elevation of cytosolic Ca2+ derived from intracellular stores via activation of the phosphatidylinositol pathway was investigated. Using an inositol 1,4,5-trisphosphate (InsP3)-specific competitive binding assay, measurable levels of InsP3 were detected in hepatopancreas and muscle in both N. norvegicus and C. maenas. Incubation of these tissues in the presence of sinus gland extracts (two sinus gland equivalents) consistently increased InsP3. In addition, Carcinus CHH (10 nM) increased InsP3 levels in Carcinus hepatopancreas and muscle. Incubation of hepatopancreas from both species in 10 mM lithium saline increased basal levels of InsP3, suggesting a significant turnover of phosphoinositides in this tissue.
PubMed ID
8921359 View in PubMed
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[Mechanisms of generating calcium signals in exocrine acinar cells]

https://arctichealth.org/en/permalink/ahliterature9995
Source
Fiziol Zh. 2001;47(6):85-96
Publication Type
Article
Date
2001
Author
P M Shevchuk
V K Rybal'chenko
Author Affiliation
Research Institute of Physiology, Taras Shevchenko Kiev University, Kiev.
Source
Fiziol Zh. 2001;47(6):85-96
Date
2001
Language
Ukrainian
Publication Type
Article
Keywords
Animals
Calcium - metabolism
Calcium Signaling - physiology
English Abstract
Exocrine Glands - cytology - metabolism
Inositol 1,4,5-Trisphosphate - metabolism
Mice
Abstract
Review. Modern data about mechanisms of generation of the calcium signals in the exocrine acinar cells are presented. The mechanisms of inositol-1,4,5-trisphosphate- and Ca(2+)-induced Ca2+ release from intracellular stores of the acinar cells and mechanisms their influx from extracellular medium are described. The mechanisms which initiate Ca2+ oscillations and their role in the secretion of the fluid and enzymes by acinar cells are discussed.
PubMed ID
11962097 View in PubMed
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Phospholipase C, but not InsP3 or DAG, -dependent activation of the muscarinic receptor-operated cation current in guinea-pig ileal smooth muscle cells.

https://arctichealth.org/en/permalink/ahliterature9572
Source
Br J Pharmacol. 2004 Jan;141(1):23-36
Publication Type
Article
Date
Jan-2004
Author
Alexander V Zholos
Yaroslav D Tsytsyura
Dmitri V Gordienko
Vladimir V Tsvilovskyy
Tom B Bolton
Author Affiliation
Department of Nerve-Muscle Physiology, A.A. Bogomoletz Institute of Physiology, Kiev 01024, Ukraine. zholosa@sghms.ac.uk
Source
Br J Pharmacol. 2004 Jan;141(1):23-36
Date
Jan-2004
Language
English
Publication Type
Article
Keywords
8-Bromo Cyclic Adenosine Monophosphate - pharmacology
Adenylate Cyclase - antagonists & inhibitors
Animals
Aristolochic Acids - pharmacology
Bridged Compounds - pharmacology
Caffeine - pharmacology
Calcium - metabolism
Carbachol - antagonists & inhibitors - pharmacology
Diglycerides - metabolism - pharmacology
Estrenes - pharmacology
Guanosine Triphosphate - analogs & derivatives - antagonists & inhibitors - metabolism
Guinea Pigs
Ileum - cytology - physiology
Indoles - pharmacology
Inositol 1,4,5-Trisphosphate - metabolism
Inositol Phosphates - metabolism
Isoenzymes - antagonists & inhibitors - metabolism
Isoproterenol - pharmacology
Male
Membrane Potentials - drug effects - physiology
Muscle, Smooth - cytology - physiology
Patch-Clamp Techniques - methods
Phospholipase C - antagonists & inhibitors - metabolism
Phospholipases A - antagonists & inhibitors
Pyrrolidinones - pharmacology
Receptor, Muscarinic M2 - drug effects - physiology
Receptor, Muscarinic M3 - drug effects - physiology
Research Support, Non-U.S. Gov't
Ryanodine - pharmacology
Thiones - pharmacology
Abstract
1. In visceral smooth muscles, both M(2) and M(3) muscarinic receptor subtypes are found, and produce two major metabolic effects: adenylyl cyclase inhibition and PLCbeta activation. Thus, we studied their relevance for muscarinic cationic current (mI(CAT)) generation, which underlies cholinergic excitation. Experiments were performed on single guinea-pig ileal cells using patch-clamp recording techniques under conditions of weakly buffered [Ca(2+)](i) (either using 50 microm EGTA or 50-100 microm fluo-3 for confocal fluorescence imaging) or with [Ca(2+)](i) 'clamped' at 100 nm using 10 mm BAPTA/CaCl(2) mixture. 2. Using a cAMP-elevating agent (1 microm isoproterenol) or a membrane-permeable cAMP analog (10 microm 8-Br-cAMP), we found no evidence for mI(CAT) modulation through a cAMP/PKA pathway. 3. With low [Ca(2+)](i) buffering, the PLC blocker U-73122 at 2.5 microm almost abolished mI(CAT), in some cases without any significant effect on [Ca(2+)](i). When [Ca(2+)](i) was buffered at 100 nm, U-73122 reduced both carbachol- and GTPgammaS-induced mI(CAT) maximal conductances (IC(50)=0.5-0.6 microm) and shifted their activation curves positively. 4. U-73343, a weak PLC blocker, had no effect on GTPgammaS-induced mI(CAT), but weakly inhibited carbachol-induced current, possibly by competitively inhibiting muscarinic receptors, since the inhibition could be prevented by increasing the carbachol concentration to 1 mm. Aristolochic acid and D-609, which inhibit PLA(2) and phosphatidylcholine-specific PLC, respectively, had no or very small effects on mI(CAT), suggesting that these enzymes were not involved. 5. InsP(3) (1 microm) in the pipette or OAG (20 microm) applied externally had no effect on mI(CAT) or its inhibition by U-73122. Ca(2+) store depletion (evoked by InsP(3), or by combined cyclopiazonic acid, ryanodine and caffeine treatment) did not induce any significant current, and had no effect on mI(CAT) in response to carbachol when [Ca(2+)](i) was strongly buffered to 100 nm. 6. It is concluded that phosphatidylinositol-specific PLC modulates mI(CAT) via Ca(2+) release, but also does so independently of InsP(3), DAG, Ca(2+) store depletion or a rise of [Ca(2+)](i). Our present results explain the previously established 'permissive' role of the M(3) receptor subtype in mI(CAT) generation, and provide a new insight into the molecular mechanisms underlying the shifts of the cationic conductance activation curve.
PubMed ID
14662735 View in PubMed
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