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PubMed1981

High-affinity [3H]choline accumulation in cultured human skin fibroblasts.

[3H]Choline can be transported across cell membranes by high-affinity (KT less than 5 microM) and low-affinity (KT much greater than 5 microM) systems. High-affinity choline accumulation (HACA) has been demonstrated in synaptosomes made from cholinergic brain regions such as the hippocampus and caudate-putamen. In cell culture, HACA has been demonstrated in glia and avian telencephalon, dissociated spinal cord, and muscle fibroblasts. We examined [3H]choline accumulation in a single normal human fibroblast line cultured from skin biopsy. [3H]Choline accumulation was temperature-dependent and linear with incubation time up to 6 min at 0.125 microM-choline. The apparent KT for [3H]choline was 5 microM, which is similar to that observed in avian fibroblasts. Isoosmotic replacement of Na+ with either Li+ (144 mM) or sucrose (288 mM) severely reduced [3H]choline accumulation (by 70-90%). Pre-incubation with ouabain (100 microM), sodium orthovanadate (100 microM), or 2,4-dinitrophenol (100 microM), or replacement of Ca2+ by Mg2+ had little or no effect on subsequent [3H]choline accumulation. [3H]Choline accumulation was inhibited by hemicholinium-3 (HC-3); after pre-incubation in HC-3 at 37 degrees C for 10 min, the IC50 (at 0.125 microM-choline) was 5.6 microM. The HC-3 sensitivity, Na+ dependence, and low KT suggest that human skin fibroblasts have a high-affinity transport system for choline.

Adult↗
PubMed1989

Acute choline supplementation in vivo enhances acetylcholine synthesis in vitro when neurotransmitter release is increased by potassium.

The main objective of these studies was to determine whether the acute administration of choline to rats provides supplemental precursor that can be used to support acetylcholine synthesis when the demand for choline is increased by increasing neurotransmitter release. For these experiments, hippocampal and striatal slices were prepared form rats that had received saline or an acute injection of choline. Slices were incubated in a choline-free buffer containing 4.74-35 mM KCl, and acetylcholine synthesis and release and choline production were measured. The initial tissue contents of acetylcholine and choline did not differ between experimental groups for either brain region. When hippocampal slices from the controls were incubated for 10 min with depolarizing concentrations of KCl, acetylcholine release increased and the tissue content decreased in a concentration-dependent fashion; no net synthesis of acetylcholine occurred. In contrast, hippocampal slices from the choline-injected animals maintained their tissue content in the presence of high concentrations of KCl, despite an increase in acetylcholine release that was similar in magnitude to that of the controls; positive net synthesis of acetylcholine resulted. Although the molar concentration of choline achieved in the incubation media at the end of the 10-min period did not differ between groups, the mobilization of free choline from bound stores was significantly greater in hippocampal slices from the choline-injected group than the controls. In addition, the synthesis of acetylcholine by hippocampal slices from the choline-injected group was prevented by the presence of hemicholinium-3 (1 microM) in the media.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1990

Effects of choline administration on in vivo release and biosynthesis of acetylcholine in the rat striatum as studied by in vivo brain microdialysis.

The purpose of the present study is to clarify the effects of the administration of choline on the in vivo release and biosynthesis of acetylcholine (ACh) in the brain. For this purpose, the changes in the extracellular concentration of choline and ACh in the rat striatum following intracerebroventricular administration of choline were determined using brain microdialysis. We also determined changes in the tissue content of choline and ACh. When the striatum was dialyzed with Ringer solution containing 10 microM physostigmine, ACh levels in dialysates rapidly and dose dependently increased following administration of various doses of choline and reached a maximum within 20 min. In contrast, choline levels in dialysates increased after a lag period of 20 min following the administration. When the striatum was dialyzed with physostigmine-free Ringer solution, ACh could not be detected in dialysates both before and even after choline administration. After addition of hemicholinium-3 to the perfusion fluid, the choline-induced increase in ACh levels in dialysates was abolished. Following administration of choline, the tissue content of choline and ACh increased within 20 min. These results suggest that administered choline is rapidly taken up into the intracellular compartment of the cholinergic neurons, where it enhances both the release and the biosynthesis of ACh.

Acetylcholine↗
PubMed1992

Ouabain-sensitive choline transport system in capillaries isolated from bovine brain.

In physiological conditions, there is a net transport of choline from brain to blood, despite the fact that the choline concentration is higher in plasma than in CSF. Because of the blood-brain barrier characteristics, such passage against the concentration gradient takes place necessarily through endothelial cells. To get a better understanding of this phenomenon, [3H]choline uptake properties have been analyzed in capillaries isolated from bovine brain. [3H]Choline uptake was linear with time for up to 1 h. Nonlinear regression analysis of the uptake rates at different substrate concentrations gave the best fit to a system of two components, one of which was saturable (Km = 17.8 +/- 4.8 microM; Vmax = 11.3 +/- 3.4 pmol/min/mg of protein) and the other of which was nonsaturable at concentrations up to 200 microM. The [3H]choline transport was significantly reduced in the absence of sodium and after incubation with 10(-4) M ouabain for 30 min. Ouabain also inhibited choline uptake in purified cerebral endothelial cells, but not in the endothelium isolated from bovine aorta. Accordingly, cerebral endothelial cells were able to concentrate [3H]choline, with this effect being abolished by ouabain, whereas in aortic endothelial cells the [3H]choline intracellular concentration was never higher than that of the incubation medium. These results suggest that the blood-brain barrier endothelium is specifically provided with an energy-dependent choline transport system, which may explain the choline efflux from the brain and the maintenance of a low choline concentration in the cerebral extracellular space.

3-O-Methylglucose↗
PubMed2004

CDP-choline increases plasma ACTH and potentiates the stimulated release of GH, TSH and LH: the cholinergic involvement.

In the present study, we investigated the effect of intracerebroventricular (i.c.v.) administration of cytidine-5'-diphosphate (CDP) choline on plasma adrenocorticotropin (ACTH), serum growth hormone (GH), thyroid stimulating hormone (TSH), follicle stimulating hormone (FSH) and luteinizing hormone (LH) levels in conscious rats. The involvement of cholinergic mechanisms in these effects was also determined. In basal conditions, CDP-choline (0.5, 1.0 and 2.0 micromol, i.c.v.) increased plasma ACTH levels dose- and time-dependently, but it did not affect the TSH, GH, FSH and LH levels. In stimulated conditions, i.c.v. administration of CDP-choline (1 micromol, i.c.v.) produced an increase in clonidine-stimulated GH, thyrotyropin-releasing hormone (TRH)-stimulated TSH, LH-releasing hormone (LHRH)-stimulated LH, but not FSH levels. Injection of equimolar dose of choline (1 micromol, i.c.v.) produced similar effects on hormone levels, but cytidine (1 micromol, i.c.v.) failed to alter plasma levels of these hormones. Pretreatment with hemicholinium-3, a neuronal high affinity choline uptake inhibitor, (20 microg, i.c.v.) completely blocked the observed hormone responses to CDP-choline. The increase in plasma ACTH levels induced by CDP-choline (1 micromol, i.c.v.) was abolished by pretreatment with mecamylamine, a nicotinic receptor antagonist, (50 microg, i.c.v.) but not atropine, a muscarinic receptor antagonist, (10 microg, i.c.v.). The increase in stimulated levels of serum TSH by CDP-choline (1 micromol, i.c.v.) was blocked by atropine but not by mecamylamine pretreatment. However, CDP-choline induced increases in serum GH and LH levels were greatly attenuated by both atropine and mecamylamine pretreatments. The results show that CDP-choline can increase plasma ACTH and produce additional increases in serum levels of TSH, GH and LH stimulated by TRH, clonidine and LHRH, respectively. The activation of central cholinergic system, mainly through the presynaptic mechanisms, was involved in these effects. Central nicotinic receptors solely mediated the increase in plasma ACTH levels while the activation of central muscarinic receptors was involved in the increase in TSH levels. Both muscarinic and nicotinic receptor activations, separately, mediated the increases in serum GH and LH levels after CDP-choline.

Adrenocorticotropic Hormone↗
PubMed1982

Effect of potassium depolarization and preganglionic nerve stimulation on the metabolism of [3H]-choline in rat isolated sympathetic ganglia.

1 The effects of potassium depolarization and preganglionic nerve stimulation on the metabolism of [(3)H]-choline in the isolated superior sympathetic ganglion of the rat have been studied.2 When unstimulated (resting) ganglia were incubated for 10 min with a low concentration (0.1 muM) of [(3)H]-choline (high affinity uptake), approximately 75% of the accumulated radioactivity was present as [(3)H]-phosphorylcholine, 11% was [(3)H]-acetylcholine ([(3)H]-ACh) and the remainder was unchanged [(3)H]-choline.3 Depolarization of the ganglia with K (46 mM) before their incubation with [(3)H]-choline, increased [(3)H]-choline uptake by 70% and increased [(3)H]-ACh synthesis by more than 700%, so that [(3)H]-ACh represented almost 50% of the total radioactivity recovered. In contrast, the proportion of [(3)H]-phosphorylcholine fell to 36% of the total radioactivity recovered.4 The striking effect of K-depolarization on [(3)H]-ACh synthesis in ganglia occurred at a concentration of 30 mM or above, and the maximum effect was seen at 45-50 mM.5 Chronic denervation of the ganglia abolished all the effects of high-K on [(3)H]-choline metabolism. In resting ganglia, [(3)H]-ACh formation was reduced by over 80% but [(3)H]-phosphorylcholine synthesis and the level of unchanged [(3)H]-Ch were not affected by denervation.6 Exposure of the ganglia to low-Na or hemicholinium-3 (HC-3) greatly reduced [(3)H]-ACh synthesis in control resting ganglia and almost abolished the effects of high-K on [(3)H]-ACh synthesis.7 Prevention of transmitter release with high-Mg or low-Ca medium also prevented K-depolarization from stimulating [(3)H]-ACh synthesis.8 Preganglionic nerve stimulation had an effect on [(3)H]-choline metabolism similar to that of K-depolarization. Thus, at all the frequencies studied (1-30 Hz), [(3)H]-ACh synthesis was greatly increased and [(3)H]-phosphorylcholine was reduced, the maximum effects occurring at 3 Hz.9 When ganglia were incubated with a high concentration (100 muM) of [(3)H]-choline (low affinity uptake), a different pattern of metabolism was observed. Most of the radioactivity in resting ganglia was present as unchanged [(3)H]-choline (70%) with [(3)H]-phosphorylcholine and [(3)H]-ACh representing 23% and 6% of the total radioactivity respectively. K-depolarization decreased [(3)H]-choline uptake but increased the proportions of [(3)H]-phosphorylcholine and [(3)H]-ACh to 32% and 24% of the total radioactivity respectively.10 It is concluded that in unstimulated (resting) rat sympathetic ganglia most of the [(3)H]-choline transport and metabolism occurs in postsynaptic structures. However, depolarization of the presynaptic nerve terminals appears to trigger a sodium-dependent, HC-3 sensitive, high-affinity uptake process, and causes a dramatic increase in presynaptic [(3)H]-ACh synthesis together with a fall in postsynaptic [(3)H]-phosphorylcholine synthesis. These changes in choline metabolism cannot be due to the depolarization of the nerve terminals per se, because they were abolished by high-Mg or low-Ca, i.e. when transmitter release was prevented. Thus, the increase in ACh synthesis may be triggered by a fall in the intraterminal concentration of ACh or by the changes in Ca flux induced by depolarization. Our experiments do not provide evidence on these possible mechanisms.

Animals↗
PubMed1995

Restoration of blood pressure by choline treatment in rats made hypotensive by haemorrhage.

1. Intracerebroventricular (i.c.v.) injection of choline (25-150 micrograms) increased blood pressure in rats made acutely hypotensive by haemorrhage. Intraperitoneal administration of choline (60 mg kg-1) also increased blood pressure, but to a lesser extent. Following i.c.v. injection of 25 micrograms or 50 micrograms of choline, heart rate did not change, while 100 micrograms or 150 micrograms i.c.v. choline produced a slight and short lasting bradycardia. Choline (150 micrograms) failed to alter the circulating residual volume of blood in haemorrhaged rats. 2. The pressor response to i.c.v. choline (50 micrograms) in haemorrhaged rats was abolished by pretreatment with mecamylamine (50 micrograms, i.c.v.) but not atropine (10 micrograms, i.c.v.). The pressor response to choline was blocked by pretreatment with hemicholinium-3 (20 micrograms, i.c.v.). 3. The pressor response to i.c.v. choline (150 micrograms) was associated with a several fold increase in plasma levels of vasopressin and adrenaline but not of noradrenaline and plasma renin. 4. The pressor response to i.c.v. choline (150 micrograms) was not altered by bilateral adrenalectomy, but was attenuated by systemic administration of either phentolamine (10 mg kg-1) or the vasopressin antagonist [beta-mercapto-beta,beta-cyclopenta-methylenepropionyl1, O-Me-Tyr2,Arg8]-vasopressin (10 micrograms kg-1). 5. It is concluded that the precursor of acetylcholine, choline, can increase and restore blood pressure in acutely haemorrhaged rats by increasing central cholinergic neurotransmission. Nicotinic receptor activation and an increase in plasma vasopressin and adrenaline level appear to be involved in this effect of choline.

Animals↗
PubMed1972

Extracellular cations and the movement of choline across the erythrocyte membrane.

1. The ability of human erythrocytes to accumulate choline is abolished when external Na is replaced by Cs, Rb, K or Li but is increased when the external cation is Mg or Ca.2. The unidirectional influx of choline is reduced when external Na is replaced by other monovalent cations but is not changed when Na is replaced by Mg or Ca.3. The unidirectional efflux of choline into a choline-free medium is increased when external Na is replaced by other monovalent cations and markedly reduced when Na is replaced by Mg or Ca. When the external medium contains 1 mM choline, changing the external cation has virtually no effect on the rate of choline efflux.4. When the extracellular concentrations of K and Na are similar to that found in the intracellular water, choline appears to become passively distributed across the cell membrane; when the extracellular K is then replaced by Cs a net efflux of choline against a concentration gradient results.5. It is concluded that the choline carrier may be described as a cation carrier with a high affinity for choline and affinities for Cs > Rb > K > Li > Na and that these monovalent cations can cross the membrane on the choline transport system.

Biological Transport, Active↗
PubMed2000

The effects of choline supplementation on physical performance.

It has been reported that plasma choline levels decrease following certain types of strenuous exercise. Preliminary findings also suggest that a drop in plasma choline may limit physical performance, while choline supplementation may delay fatigue during prolonged efforts. A double-blind crossover design was used to determine the relationship between plasma choline and performance during and after 4 hr of strenuous exercise. Volunteers (N = 14) received either a placebo or treatment beverage (8.425 g choline citrate) prior to and midway through a 4-hr load carriage treadmill exercise (3% grade at 5.6 km/h 3 20 km) carrying a total load of 34.1 kg. Following the treadmill test, run time-to-exhaustion and squat tests were performed, and perceived exertion, plasma choline, glycerophosphocholine, and phosphatidylcholine were measured. Plasma choline levels increased 128% after the run-to-exhaustion with the choline supplemented beverage but remained unchanged with the placebo beverage. No significant effects were seen with choline supplementation on any outcome performance measure. Consequently, soldiers conditioned to carry heavy loads over long distances do not deplete plasma choline as a result of a prolonged exhaustive exercise under a placebo beverage, nor do they benefit from choline supplementation to delay fatigue under the same conditions.

Adult↗
PubMed1993

Choline transport activity in Staphylococcus aureus induced by osmotic stress and low phosphate concentrations.

Uptake of [14C]choline upon hyperosmotic stress of exponential-phase Staphylococcus aureus cultures in a complex medium occurred after a delay of 2.5 to 3.5 h. This uptake could be prevented by chloramphenicol, suggesting that it occurred via an inducible transport system. Radioactivity from [14C]choline was accumulated as [14C]glycine betaine. However, neither choline nor glycine betaine could act as the major carbon and energy source for the organism, suggesting that choline was not metabolized beyond glycine betaine. Assay of choline transport activity in cells grown under different conditions in defined media revealed that osmotic stress was mainly responsible for the induction, but choline gave a further increase in induction. The system was not induced in anaerobically grown cells. Choline transport activity was repressed by glycine betaine and proline betaine, suggesting that these compounds are corepressors. Choline transport activity was not induced in cells osmotically stressed by 1 M potassium phosphate or 0.5 M sodium phosphate, but was induced in cells grown in low-phosphate medium in the absence of osmotic stress. This suggests that there is a connection between the phosphate and osmotic stress regulons. Choline transport was energy and Na+ dependent and had a Km of 46 microM and a maximum rate of transport (Vmax) of 54 nmol/min/mg (dry weight). The results of competition studies suggested that N-methyl and an alcohol group or aldehyde groups at the ends of the molecule were important in its recognition by the system. Glycine betaine was not a highly effective competitor, suggesting that its transport system and the choline transport system were distinct from each other. Choline transport was highly susceptible to a variety of inhibitors, which may be related to the greater dependence on respiratory metabolism of cells grown in the presence of high NaC1 concentrations.

Biological Transport↗
PubMed1994

Na(+)-dependent and Na(+)-independent systems of choline transport by plasma membrane vesicles of A549 cell line.

Membrane vesicles of A549 lung cells accumulate choline by two pathways: the Na(+)-independent uphill uptake of choline [Michaelis-Menten constant (Km) approximately 44 microM; steady-state gradient approximately 45 at 5 microM external choline] is dependent on a transmembrane H+ gradient, is relatively insensitive to hemicholinium-3, is amiloride sensitive, and is abolished by valinomycin plus carbonyl cyanide p-trifluoromethoxyphenylhydrazone (FCCP). The Na(+)-dependent active choline uptake (Km approximately 4 microM, inhibitor constant for hemicholinium-3 approximately 0.1 microM), is specific for Na+, is amiloride and FCCP sensitive, and is electrogenic: the overshoot using K(+)-loaded vesicles and NaCl gradient was increased by valinomycin. The time of the overshoot peak, T was approximately 90 s in a NaSCN medium (or in presence of other lipid-soluble anions), a value close to that for alpha-aminoisobutyrate as substrate (T = approximately 1.5 min). T was lengthened in NaCl medium to approximately 10 min, and the overshoot was abolished by impermeant anions. External Cl- is not required for the choline uptake: valinomycin produced an overshoot in the presence of only impermeant anions, with T approximately 90 s. Most of the above properties are shared by the high-affinity Na(+)-dependent choline transport in synaptosomes. The characteristics of the Na(+)-dependent choline uptake by membrane vesicles of A549 cells are consistent with an electrogenic choline(+)-Na+ cotransport, with the rate-limiting anion (e.g., Cl-) influx balancing the positive charges transferred into the vesicles. The data are also consistent with an involvement of an amiloride-sensitive choline+/H+ antiport (or choline(+)-OH- symport) in the low- and high-affinity choline uptake pathways.

Anions↗
PubMed1986

Choline evokes fluid secretion by perfused rat mandibular gland without desensitization.

The secretomotor action of choline on salivary secretion has been studied in the isolated perfused mandibular gland of the rat. Choline made up in substituted Ringer solutions (Na concentrations of 40, 70, or 100 mM) was an effective secretomotor agonist in the concentration range of 1-100 mM and evoked secretory responses comparable with those of acetylcholine (0.05-1.0 microM) administered at similar Na concentrations. Continuous infusion of choline, in contrast to acetylcholine, did not lead to a fall off in the secretory response (desensitization or tachyphylaxis) until the choline concentration used exceeded approximately 80 mM. The secretomotor action of choline (46 mM) was blocked completely and reversibly by atropine (5 microM) but not by propranolol (2.5 microM) and phentolamine (2.5 microM) administered together. When acetylcholine (1.0 or 0.05 microM) was infused on a background of choline stimulation, a small additional secretory response was elicited whenever the choline stimulus was submaximal, and, regardless of the choline concentration employed, addition of acetylcholine always induced tachyphylaxis. The results suggest that choline and acetylcholine act on the same population of muscarinic receptors, but it is unclear why choline does not evoke tachyphylaxis. The response to choline allows us to exclude a number of the possible causes of tachyphylaxis that have previously been considered, so that an excessive buildup of cytosolic free Ca now remains as the most likely cause of the phenomenon.

Acetylcholine↗
PubMed1998

A choline-rich diet improves survival in a rat model of endotoxin shock.

This study investigated whether dietary choline can prevent endotoxin shock. Female Sprague-Dawley rats fed chow or chow plus choline chloride (0.025-0.4%) for 3 days were given lipopolysaccharide (LPS) via the tail vein. Eighty-three percent and 56% of chow-fed rats survived after 2.5 or 5.0 mg/kg LPS, respectively. Choline increased survival in a dose-dependent manner, with maximal effects observed at 0.4%; this dose of choline prevented mortality completely after 2.5 or 5 mg/kg LPS. Choline also improved the microscopic appearance of the lungs and blunted increases in serum aspartate aminotransferase levels. Intracellular Ca2+ was monitored in liver and lung macrophages during LPS exposure. Ca2+ increases in macrophages from choline-fed rats were blunted by 40-60% compared with chow-fed controls. Feeding choline also blunted tumor necrosis factor-alpha production. Feeding glycine, which prevents macrophage activation via a chloride channel, in addition to choline was even more effective than feeding choline alone, suggesting that glycine and choline act via distinct sites. These data are consistent with the hypothesis that choline diminishes endotoxin shock by preventing macrophage activation.

Animals↗
PubMedDate not supplied

Plasma choline concentrations in children requiring long-term home parenteral nutrition: a case control study.

BACKGROUND: Low plasma free choline concentration has been associated with elevated serum hepatic aminotransferase concentrations and hepatic steatosis in adults who need home parenteral nutrition (HPN). We sought to determine if plasma free choline is similarly reduced in children who need home total parenteral nutrition (TPN). METHODS: We compared the plasma free choline concentration in 21 children who required long-term HPN with 31 normal controls. Patients had received HPN for 75 +/- 13 (SD) months (range 3-206 months). All control children ingested a normal, mixed, nonvegetarian diet. RESULTS: The mean plasma free choline concentration in the children receiving HPN was significantly lower than normal children (6.6 +/- 4.3 vs 8.0 +/- 2.3 nmol/mL, p = .002). Plasma free choline concentration was correlated with age (r = -0.43, p = .049). Using multiple linear regression analysis for age, sex, and squared age (considered in order to account for possible nonlinearity between choline and age), HPN children showed a steady and significant decline in plasma free choline concentration with increased age at the rate of 0.03 nmol/mL per month. Plasma lipid bound choline concentration did not vary with age. No relationship was seen between either plasma free and lipid bound choline concentration and amount of daily IV lipid infusion. A significant negative correlation was observed between plasma free choline concentration and aspartate aminotransferase (AST) and alanine aminostransferase (ALT) (r = -0.72, p = .04 and r = -0.80, p = .02, respectively). CONCLUSION: Our data support the notion that patients who need long-term HPN without significant enteral feeding have a significant risk for the development of choline deficiency with its associated hepatic dysfunction.

Adolescent↗
PubMed1991

Pharmacological characteristics of choline transport system in mouse cerebral cortical neurons in primary culture.

The characteristics of [3H]choline transport with high affinity were investigated using primary cultured neurons obtained from the mouse cerebral cortex. [3H]Choline uptake was saturable as a function of extracellular [3H]choline concentration. Analysis by Lineweaver-Burk plot revealed that [3H]choline was transported into neurons by a high affinity transport system with a Km value of 19.8 +/- 0.8 microM and Vmax value of 0.334 +/- 0.022 nmol/mg protein/min. This high affinity transport of [3H]choline was significantly inhibited by the withdrawal of sodium from the incubation medium, incubation at low temperature (4 degrees C) and addition of metabolic inhibitors such as monoiodoacetate. These results indicate that the high affinity [3H]choline uptake in primary cultured neurons is sodium- and energy-dependent. Hemicholinium-3 also showed a competitive inhibition on the [3H]choline transport. Depolarization by high K+ induced an enhancement of the [3H]choline uptake in the presence of Ca2+. The crude synaptosomal fraction obtained from primary cultured neurons possessed approximately forty-fold higher synthesizing activity of [3H]acetylcholine from [3H]choline than that found in the homogenate preparation of cultured neurons. The present results strongly suggest that the primary cultured neurons used in this study possess a sodium- and energy-dependent high-affinity choline uptake system as well as a synthesizing system for acetylcholine. Possible usefulness of these neurons for investigating neuronal uptake of choline and its functional role in the biosynthesis of acetylcholine are also suggested.

Acetylcholine↗
PubMed1982

Mechanism of choline-induced secretion of catecholamines from the cat adrenal medulla: involvement of nicotinic receptor.

Cat adrenal glands were retrogradely perfused in vitro with modified Locke's medium and the mechanism of catecholamine (CA) secretion induced by choline was investigated. Choline-induced secretion of CA was accompanied by release of dopamine-beta-hydroxylase, but not by that of phenylethanolamine-N-methyl transferase, indicating that an exocytotic mechanism is involved in the secretion. Choline failed to induce the secretion of CA when Ca was absent from the perfusion solution. On the other hand, secretion increased when the concentration of Ca2+ in the perfusion medium was raised to 10 mM. Stimulation of secretion by choline was observed from a concentration of 1 mM, and half-maximal secretion occurred at about 10 mM. The stimulatory action was weaker than that of acetylcholine(ACh); the effect of 100 mM choline was approximately equal to that of 0.02 mM ACh. Secretion induced by a low concentration of choline was abolished by a nicotinic blocker, hexamethonium, while the response to choline at a concentration higher than 130 mM was only partially inhibited by cholinergic antagonists. The effects of choline and a low concentration of ACh were additive. On the other hand, 100 mM choline inhibited the response to a supramaximal concentration of ACh(0.5 mM), suggesting that ACh and choline stimulate the same nicotinic receptor. It is concluded that choline acts partially as a nicotinic agonist and that a concentration higher than 130 mM causes secretion by a mechanism additional to nicotinic receptor activation.

Acetylcholine↗
PubMed1991

Effect of dietary rumen-protected choline in lactating dairy cows.

Two experiments were conducted to test the effects of graded amounts of rumen-protected choline on milk yield and composition in lactating dairy cows fed 40% corn silage and 60% concentrate diets (DM basis). In Experiment 1, 48 Holstein cows were fed 0, .078, .156, and .234% rumen-protected choline (choline chloride basis) from wk 5 to 21 postpartum. Increasing choline had no effect on DMI and tended to increase milk yield only from 1 to 2.2 kg/d. Milk fat percentage was reduced in the .078% choline treatment and increased to control levels thereafter with .156 and .234% choline. In Experiment 2, 16 Holstein cows in midlactation were assigned randomly to either 13.0 or 16.5% dietary CP (DM basis). Within CP concentration, cows were fed 0, .08, .16, and .24% rumen-protected choline in a replicated 4 x 4 Latin square design. Dietary protein had no effect on milk yield, although milk protein percentage and yield were increased .25 percentage units and 63 g/d, respectively, by increased dietary CP. Increasing dietary choline to .24% linearly increased milk yield 2.6 kg/d, although it had no consistent effects on milk fat or protein percentage. There was only a slight tendency for greater responses in milk yield to dietary choline with lower dietary CP. Data from these experiments confirm earlier results with postruminal choline infusions, suggesting that choline may be a limiting nutrient for milk production.

Animal Feed↗
PubMed1975

Reproductive performance of caged Beltsville Small White turkeys as affected by choline, bird density and forced molting.

Reproductive performance was determined on Beltsville Small White hens housed 2 or 3 per cage for 10 weeks and then changed to 1 or 2 per cage for 10 additional weeks. Hens were then molted and data collected for a second production cycle of 18 weeks. Hens were fed a basal diet calculated to contain 1230 mg./kg. of choline, or supplemented with choline chloride to provide 1900, 2570 or 3240 mg. of choline per kg. of diet. Variations in production, fertility and hatch were observed between the first and second 10 week periods of the first laying cycle, but differences were affected more by two high choline levels than by number of hens per cage. When data was combined to show the effects of choline supplements for the entire 20 weeks, there were no significant differences in egg production or hatch of fertile eggs due to choline levels. However, significantly lower fertility resulted in groups fed choline at the level of 2570 or 3240 mg./kg. during this 20 wk. laying cycle. During the second production cycle (one hen per cage), choline supplements improved egg production, increased egg weight, depressed fertility and had no effect on hatch of fertile eggs. When data from the first and second production cycles were combined, there was no significant effect of choline on production or hatchability, but all groups supplemented with choline had significantly lower fertility than the basal group, indicating that 1230 mg./kg. of choline was adequate.

Animals↗