3,4-Diaminopyridine and choline increase in vivo acetylcholine release in rat striatum

Büyükuysal, R. Levent; Ulus, İsmail H.; Aydin, Sami; Kiran, B.K.

doi:10.1016/0014-2999(95)00241-c

Cited by 34 publications

(12 citation statements)

References 29 publications

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“…Platelet functions [as collagen adenosine diphosphate-closure time (CADP-CT) and collagen epinephrine-closure time (CEPI-CT)] were analyzed at 0.5 h after treatments with Platelet Function Analyzer (PFA-100 TM ; Dade Behring, Marburg, Germany), as described previously [11]. Serum-free choline was extracted and assayed, as described previously [9,11,19].…”

Section: Methodsmentioning

confidence: 99%

“…Cells were suspended in 1 ml of ice-cold distilled water and homogenized with ultrasonic cells disrupter; homogenates were centrifuged at 14 250g for 2 min. The supernatant was used for choline and acetylcholine assay by high-pressure liquid chromatography-electrochemical (HPLC-EC) detection system (Agilent 1100 Series HPLC-EC system, Agilent Technologies, Inc., California, USA) combined with an immobilized enzyme reactor (ACh/Ch assay column Kit, MF-8910; Bioanalytical System Inc., Indiana, USA) as described previously [19]. The pellets were then re-homogenized in a sufficient volume of 50 mmol/l sodium/potassium phosphate buffer (pH ¼ 7.…”

Section: Methodsmentioning

confidence: 99%

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Choline or CDP-choline attenuates coagulation abnormalities and prevents the development of acute disseminated intravascular coagulation in dogs during endotoxemia

Yılmaz

Özarda²,

Cansev³

et al. 2010

Blood Coagulation & Fibrinolysis

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Sepsis/endotoxemia causes platelet dysfunctions, abnormalities in coagulation and hemostatic mechanisms leading to organ dysfunctions and mortality. Choline prevents organ injury and improves survival during endotoxemia. The main objective of the present study was to determine the effects of choline or cytidine-5'-diphosphocholine (CDP-choline) on endotoxin-induced activation of coagulation and development of disseminated intravascular coagulation (DIC). Dogs were treated intravenously (i.v.) with saline, choline (20 mg/kg), or CDP-choline (70 mg/kg) three times with 4-h intervals starting 5 min before i.v. injection of endotoxin (1 mg/kg). Platelet counts and functions, prothrombin time (PT), activated partial thromboplastin time (aPTT), fibrinogen, coagulation factors, D-dimer and antithrombin (AT) were measured before and at 0.5-96 h after endotoxin. Circulating platelet, fibrinogen, coagulation factors and AT were decreased, whereas PT and aPTT were prolonged and serum D-dimer levels were elevated after endotoxin. Endotoxin-induced reductions in platelet counts and functions, fibrinogen, coagulation factors and AT were attenuated or blocked by choline or CDP-choline. Choline or CDP-choline blocked endotoxin-induced prolongation in PT and aPTT and enhancement in D-dimer. Elevated DIC scores were attenuated by choline and blocked by CDP-choline. Choline administration increased serum choline concentrations and caused bradycardia. Choline also increased choline and acetylcholine contents of circulating mononuclear cells and inhibited radioligand binding to their cholinergic receptors. These data show that choline administration, as choline chloride or CDP-choline, restores the abnormalities in the primary, secondary, and tertiary hemostasis and prevents the development of DIC during experimental endotoxemia in dogs probably by increasing both neuronal and non-neuronal cholinergic activity.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Choline or CDP-choline attenuates coagulation abnormalities and prevents the development of acute disseminated intravascular coagulation in dogs during endotoxemia

Yılmaz

Özarda²,

Cansev³

et al. 2010

Blood Coagulation & Fibrinolysis

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“…Phosphocholine and glycerophosphocholine were first hydrolyzed enzymatically to free choline by using specific enzymes, namely, alkaline phosphatase for phosphocholine [25,26] and glycerophosphocholine phosphodiesterase for glycerophosphocholine [27], and the resulting choline was assayed by high-performance liquid chromatographyelectrochemical detection system as described previously [28]. The dried aqueous phase of the extracted serum or milk samples was redissolved in 400 of Tris-HCl buffer (50 mM; pH = 8.0) containing 1 mM MgCl 2 .…”

Section: Extraction and Chemical Analysismentioning

confidence: 99%

Choline status in newborns, infants, children, breast-feeding women, breast-fed infants and human breast milk

İlçöl

Özbek

Hamurtekin

et al. 2005

The Journal of Nutritional Biochemistry

157

147

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“…This drug acts by blocking presynaptic M2 muscarinic receptors (Westerink et al, 1990;Buyukuysal et al, 1995;Oo et al, 1996;Moor et al, 1998). In the first 2 microdialysis experiments, four samples were collected from each rat to establish the baseline extracellular ACh levels; striatal ACh tissue content was measured among the rats of the second experiment.…”

Section: Microdialysismentioning

confidence: 99%

Dietary supplementation with uridine-5′-monophosphate (UMP), a membrane phosphatide precursor, increases acetylcholine level and release in striatum of aged rat

2007

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The biosynthesis of brain membrane phosphatides, e.g., phosphatidylcholine (PtdCho), may utilize three circulating compounds: choline, uridine (a precursor for UTP, CTP, and CDP-choline), and a PUFA (e.g., docosahexaenoic acid); moreover oral administration of the uridine source uridine-5′-monophosphate (UMP) can significantly increase levels of the phosphatides throughout the rodent brain. Since PtdCho can provide choline for acetylcholine (ACh) synthesis, we determined whether UMP administration also affects ACh levels in striatum and striatal extracellular fluid, in aged and young rats. Among aged animals consuming a UMP-containing diet (2.5%, w/w) for 1 or 6 weeks, baseline ACh levels in striatal dialysates rose from 73 fmol/min to 148 or 197 fmol/min (P<0.05). Consuming a lower dose (0.5%) for 1 week produced a smaller but still significant increase (from 75 to 92 fmol/min, P<0.05), and elevated striatal Ach content (by 16%; P<0.05). Dietary UMP (0.5%, 1 week) also amplified the increase in ACh caused by giving atropine (10 μM in the aCSF); atropine alone increased ACh concentrations from 81 to 386 fmol/min in control rats and from 137 to 680 fmol/min in those consuming UMP (P<0.05). Young rats eating the UMP-containing diet exhibited similar increases in basal ECF ACh (from 105 to 118 fmol/min) and in the increase produced by atropine (from 489 to 560 fmol/min; P<0.05). These data suggest that giving a uridine source may enhance some cholinergic functions, perhaps by increasing brain phosphatide levels. Scope: Section 3 (Neurophysiology, Neuropharmacology and other forms of Intercellular Communication)

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3,4-Diaminopyridine and choline increase in vivo acetylcholine release in rat striatum

Cited by 34 publications

References 29 publications

Choline or CDP-choline attenuates coagulation abnormalities and prevents the development of acute disseminated intravascular coagulation in dogs during endotoxemia

Choline or CDP-choline attenuates coagulation abnormalities and prevents the development of acute disseminated intravascular coagulation in dogs during endotoxemia

Choline status in newborns, infants, children, breast-feeding women, breast-fed infants and human breast milk

Dietary supplementation with uridine-5′-monophosphate (UMP), a membrane phosphatide precursor, increases acetylcholine level and release in striatum of aged rat

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