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PubMed1981

Immune response to phosphorylcholine. VIII. The response CBA/N mice to PC-LPS.

CBA/N mice and F1 crosses of CBA/N X BALB/c with the CBA/N phenotype respond to immunization with PC-LPS with a PC-specific and an anti-bridge antibody production. The PC-specific response in defective CBA/N and NBF1 is devoid of the IgG3 subclass and is not T15 idiotype dominant, whereas normal BALB/c and nondefective NBF1 mice express the T15 dominantly in their anti-PC-LPS response. By the criteria of responsiveness to PC-LPS only and the absence of dominant T15 expression, the precursors in defective NBF1 mice for TI-1 antigen PC-LPS can be characterized as being immature B cells similar to those found in neonatal livers of normal BALB/c or in spleens of chronically idiotype suppressed BALB/c mice. This analogy suggests that the developmental defect in CBA/N mice becomes active during the maturation process before selection for clonal dominance occurs and specialization of precursors for the preferred expression of the IgG3 subclass is completed. Alterations in the T cell compartment may contribute to the immature nature of B cells in the sex-linked immunodeficiency of CBA/N mice.

Aging↗
PubMed1976

Effects of essential fatty acid deficiency and carbon tetrachloride-induced liver cirrhosis on lipid and fatty acid compositions of oral palatal epithelium in rats.

Lipid pattern and fatty acid composition of oral palatal epithelium were investigated in three groups of Sprague-Dawley rats: essential fatty acid (EFA)-deficient rats, which were fed diets containing 0.07 calorie% EFA for more than two generations; liver cirrhotic rats repeatedly injected with carbon tetrachloride; control rats fed standard pellets. The fatty acid pattern was studied in choline phosphoglycerides, ethanolamine phosphoglycerides, total phosphoglycerides, triglycerides and free fatty acids. Disturbances in the farry acid composition were seen chiefly in the EFA-deficient group, where marked reductions of the polyunsaturated fatty acids 18:2 and 20:4 (n-6) of the linolecic acid series were observed. At the same time, a compensatory increase was registered in the amount of 18:1 and 20:3 (n-9) of the oleic acid series. Corresponding findings were also found for the liver cirrhotic rats, except for the reduction of 18:2, but the changes of the fatty acid pattern in this group were not as marked as was observed for the EFA-deficient rats. In the lipid pattern no differences were seen between the three experimental groups, except for a somewhat higher content of lipid phosphorus and cholesterol in the EFA-deficient rats and a higher amount of free fatty acids in the liver cirrhotic group compared with the control rats. Changed physiological condition of the oral mucosa was suggested to be a result of the observed disturbances in the fatty acid composition of the oral epithelium.

Animals↗
PubMed1978

Cholinergic systems in muscle and brain in vitamin E-deficient rats.

Rats fed a vitamin E-deficient diet for 7--8 weeks postweaning showed no change in brain weight or the activity in brain of various enzymes involved in neurotransmitter synthesis and metabolism. Body and muscle weights were markedly reduced. Muscle choline acetyltransferase and acetylcholinesterase activities were significantly elevated on a protein basis, but the total amount of choline acetyltransferase/muscle was essentially normal and total acetylcholinesterase activity was slightly reduced. Total carnitine acetyltransferase and butyrylcholinesterase activities were markedly decreased. The results are quite different from those found in hereditary murine muscular dystrophy and suggest a myogenic etiology for the vitamin E-deficiency-induced condition.

Acetylcholinesterase↗
PubMedDate not supplied

[Content of lipids and their fractions in erythrocyte membranes of rats with Guerin's carcinoma, A-avitaminosis and the effect of vitamin A in significant doses].

The content of lipids in rat erythrocyte membranes was studied with vitamin A deficiency, Guerin's carcinoma and with administration of significant doses of vitamin A. It is found that vitamin A deficiency decreases the content of phospholipid fractions: phosphatidyl ethanolamine, sphingomyelin, phosphatidyl serine. The content of phosphatidyl choline is unchanged. Under conditions of the experiment the content of cholesterol decreases. This dependence is lost when calculating per 1 g of protein. In erythrocytes of rats with Guerin's carcinoma the content of lipids increases. The character of the results is unchanged when calculating per 1 mg of protein. When administering 200.000 IU of vitamin A the content of the phospholipid and free cholesterol identified fractions lowers significantly.

Animals↗
PubMed1986

1,25-Dihydroxyvitamin D3 treatment results in increased choline acetyltransferase activity in specific brain nuclei.

To better understand the role of 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] in brain function, the level of calcium-binding protein (CaBP) and the activities of choline acetyltransferase (CAT) and monoamine oxidase were measured in discrete brain nuclei of vitamin D-deficient and -replete male rats. The nuclei sampled were those in which receptors for 1,25-(OH)2D3 and/or vitamin D-dependent CaBP have been localized. Significant elevations in CAT activity were found in the arcuatemedian eminence and in the bed nucleus of the stria terminalis of rats made vitamin D replete by eight daily ip injections of 100 or 200 ng 1,25-(OH)2D3 as well as by constant intraventricular (ivi) infusion of 25 ng 1,25-(OH)2D3 for 7 days. The percent increase ranged from 12-45% and was related to the ip dose administered. Constant ivi of 2 mM CA2+ or 125 ng 25-hydroxyvitamin D3/day for 7 days did not alter CAT activity. No significant changes in monoamine oxidase or CaBP in discrete brain nuclei were observed with vitamin D repletion. Since the arcuate-median eminence of the hypothalamus is an important regulatory site in the neuroendocrine control of reproduction, serum testosterone was measured. Serum testosterone levels were abnormally low in the vitamin D-deficient animals, but increased 2- to 5-fold to normal values in those rats made vitamin D replete by constant ivi of 25 ng 1,25-(OH)2D3 or by ip injection of 100 or 200 ng 1,25-(OH)2D3. Patterns of serum LH paralleled those for testosterone. Our results suggest that 1,25-(OH)2D3 effects cholinergic activity in several discrete brain regions and may play a role in the neuroendocrine regulation of certain aspects of anterior pituitary gland function.

Animals↗
PubMedDate not supplied

Effect of age on behavioral and enzymatic changes during thiamin deficiency.

Open field behavior and whole brain enzymatic activities were determined during thiamin deficiency in two strains of young, as well as in aged mice. In young CD-1 mice, thiamin deficiency reduced total distance traveled and vertical movements after 7 days and the decline was more than 50% by day 9. The behavioral deficit was highly correlated to decreases in 2-oxoglutarate dehydrogenase activity (KGDH). The open field behavior of Balb/c mice was about 40% less than in CD-1 mice and responded in a qualitatively different manner to thiamin deficiency. The activity of the Balb/c mice increased and then decreased with thiamin deficiency. The activity of 3 month old mice peaked on day 6 (126% of initial score), whereas 10 and 30 month mice showed a much greater increase (about 175% of initial scores), but on day 7. Although the activity of the thiamin dependent enzyme transketolase (TK) was affected similarly at all ages, the activity of KGDH in the aged brain was more sensitive to thiamin deficiency than in the young; KGDH activity declined 41%, 57% or 74% at 3, 10, or 30 months, respectively. Thus, the current mouse model is an attractive one to study the interaction of thiamin deficiency with aging.

Aging↗
PubMed1991

Hepatic plasma membrane fluidity and dietary proteins.

Effect of protein deficient diet on hepatic plasma membrane fluidity has been studied in rats using (i) steady state fluorescence polarization and anisotropy, (ii) phospholipid and cholesterol contents, (iii) phospholipid fatty acid composition, (iv) turnover of phosphatidyl choline (PC), and (v) activities of membrane-bound enzymes as parameters and rats fed casein (20%) diet as standard group. A significant increase in steady state fluorescence and anisotropy values was registered in the deficient group, indicating increased resistance and hence decrease in fluidity of the plasma membrane. Supplementation of the diet with lysine and threonine improved these values, thereby suggesting the significance of diet for membrane fluidity. Simultaneous significant alterations in other parameters, viz. (i) decrease in PC, PE and free cholesterol and increase in esterified cholesterol contents, (ii) decrease in unsaturation of fatty acids of PC, (iii) decrease in incorporation of NaH2 32PO4, [CH3-14C]choline and [CH3-14C]methionine into plasma membrane PC, and (iv) decrease in activities of plasma membrane 5'-nucleotidase and phosphodiesterase along with increase of (Na(+)-K+)ATPase and adenyl cyclase, were observed in the deficient group which on supplementation with lysine and threonine showed improvement over alterations.

Animals↗
PubMed1973

The formation of choline O-sulphate by Pseudomonas C12B and other Pseudomonas species.

Pseudomonas C(12)B and other Pseudomonas species released larger amounts of a (35)S-labelled metabolite into the medium when cultured on growth-limiting concentrations of Na(2)SO(4) as opposed to growth in SO(4) (2-)-sufficient media. The metabolite was found at all stages of the culture cycle of Pseudomonas C(12)B and maximum quantities occurred in stationary-phase culture supernatants. The metabolite was not detected when the bacterium was cultured on growth-limiting concentrations of potassium phosphate. The amount of the metabolite present in the medium greatly exceeded that which could be extracted from intact cells and, except for choline chloride, it was independent of the carbon source used for growth. If choline chloride was present in high concentration, then larger amounts of the metabolite were found in the culture medium. The metabolite was not detected extracellularly or intracellularly when the bacterium was grown in SO(4) (2-)-deficient media containing 5mm-l-cysteine. The same metabolite was also synthesized in vitro only when Pseudomonas C(12)B extracts were incubated with choline chloride, ATP, MgCl(2) and Na(2) (35)SO(4). The metabolite-forming system was not subject to repression by Na(2)SO(4) and was completely inhibited by 0.5mm-l-cysteine and activated by Na(2)SO(4) (up to 1.0mm). The metabolite was identified as choline O-sulphate by electrophoresis, chromatography and isotope-dilution analysis. Another (35)S-labelled metabolite was also detected in culture supernatants, but was not identified.

Acetates↗
PubMed1975

The effect of retinol and retinoic acid on physiological and biochemical changes in retinol-deficient rats.

1. The effects of retinol and retinoic acid supplementation of retinol-deficient rats were studied for a variety of metabolic processes shown to be affected by retinol-deficiency. 2. Retinol-deficient rats were found to have decreased body-weight, liver and testes weights, a degeneration of testicular germinal cells, an increased incorporation of labelled choline into liver and testes phospholipids, an increased protein synthetic activity (in vitro) of liver ribosomes, an increased transfer-RNA methyltransferase activity in liver and a decreased activity in testes, an increased DNA content of testicular nuclei, and a decreased uptake of [3-H]thymidine by testicular nuclear DNA. 3. In retinol-deficient rats supplemented for 8 weeks with retinol these changes were reversed, measurements returning to control levels. 4. In retinol-deficient rats supplemented for 8 weeks with retinoic acid all changes were reversed except those in the testes. 5. Testicular signs of retinol deficiency appeared to be delayed when retinoic acid was added to the retinol-deficient diet of weanling rats. This suggests a sparing action of retinoic acid on the rat's utilization of retinol. 6. Suggestions are offered as to why retinoic acid will support growth and development but not spermatogenesis in the rat.

Animals↗
PubMed1988

Comparative chromatographic study of modifications of brush-border membrane vesicles induced by an essential fatty acid-deficient diet.

The surface properties of small intestine brush-border membranes (BBMs) were examined by frontal affinity chromatography using three types of unsolubilized ligands: phlorizin polymer, immobilized lectins and linolenic acid bound to agarose gel. BBM vesicles were purified from piglets fed a corn oil diet (control diet) or a hydrogenated coconut oil diet. The second diet was representative of a deficient supply of essential polyunsaturated fatty acid (EPUFA). It induced a marked decrease in 18:2n-6 content in membrane choline phosphoglycerides and ethanolamine phosphoglycerides, whereas 20:3n-9 appeared in each class of phospholipids. Control and EPUFA-deprived BBM vesicles bound to phlorizin polymer, linolenic acid-agarose and wheat germ agglutinin (WGA) gel. In contrast, concanavalin A gel and Lens culinaris A gel exhibited a low binding capacity towards the two types of vesicles. EPUFA deficiency induced a slight decrease in binding on phlorizin polymer and a marked increase in binding on WGA gel, whereas the two types of vesicles similarly bound to linolenic acid-agarose. Desorption of phlorizin polymer-bound membranes was performed using several detergents with special regard to sodium deoxycholate (NaDOC) micelles. Sucrase activity recovery showed that the efficiency of NaDOC desorption was diminished in the case of EPUFA-deprived vesicles. EPUFA-deprived membrane domains involved in the binding would be less sensitive to the detergent attack. This assumption agrees with the putative decrease in membrane fluidity induced by the deficient diet. The possibility that fatty acid compositional changes induced by dietary lipids are extensive enough to alter some chromatographic properties of BBM vesicles is discussed.

Animals↗
PubMed1988

Effects of intracerebroventricular injection of AF64A on learning behaviors in rats.

The effects of intracerebroventricular (ICV) injection of ethylcholine aziridinium ion (AF64A) (3 nmole/2 microliter, each lateral ventricule), a putative selective cholinotoxin, on learning behaviors and choline acetyltransferase (ChAT) activity were studied in rats. AF64A-treated rats (AF64A-rat) exhibited deficient performance in a passive avoidance task and a delayed alternation task in the T-maze, but demonstrated superior avoidance response in a two-way shuttle avoidance task. These changes in learning behaviors were associated with the selective decrease of hippocampal ChAT activity. Physostigmine (0.1 mg/kg, i.p.) significantly improved the retention latency of AF64A-rats in the passive avoidance task. AF64A-rats receiving physostigmine (0.2 mg/kg, i.p.) exhibited a slight but not significant improvement of performance in the delayed alternation task in the T-maze. These findings suggested that ICV injection of AF64A may be useful for producing an experimental amnesia model with hippocampal cholinergic hypofunction like Senile dementia of the Alzheimer type (SDAT), if appropriate learning tests are selected.

Alzheimer Disease↗
PubMed1985

Activation of the alternative complement pathway by pneumococcal lipoteichoic acid.

Cell wall teichoic acids of some gram-positive bacteria are potent activators of the alternative pathway of complement. It is unclear, however, whether the other form of teichoic acid, cell membrane lipoteichoic acid (LTA), can also activate the alternative pathway. In the present study, radiolabelled pneumococcal LTA was found to bind spontaneously to sheep erythrocytes in a temperature- and time-dependent fashion. In addition, the presence of pneumococcal LTA on the erythrocyte surface was verified by the fact that they could be agglutinated by a myeloma protein (TEPC-15) specific for choline, a constituent of pneumococcal LTA. Pneumococcal LTA when fixed to the surface of erythrocytes was able to activate the alternative pathway of complement in both guinea pig serum deficient in the fourth component of complement and human serum deficient in the second component of complement, resulting in lysis of the sensitized erythrocytes. The sensitizing principle of the LTA preparation was removed before erythrocyte sensitization by immunoabsorption, using the choline-specific TEPC-15 myeloma protein. These data demonstrate that purified pneumococcal LTA will bind to sheep erythrocytes and endow them with the ability to activate the alternative pathway.

Animals↗
PubMed2000

Lithium activates mammalian Na+/H+ exchangers: isoform specificity and inhibition by genistein.

Replacement of external NaCl with LiCl induced cytoplasmic alkalinization in CCL-39 cells and rat L6 myoblasts expressing the endogenous Na+/H+ exchanger isoform NHE1. This Li+-induced alkalinization is due to activation of the Na+/H+ exchanger because it was completely inhibited by 100 microM ethylisopropylamiloride (apparent Kd=1 microM) and because it did not occur in exchanger-deficient PS120 cells. The effect of Li+ was not mimicked by Na+, K+, Cs+ and choline+. Li+ caused cytoplasmic alkalinization in PS120 cells expressing NHE1 or NHE2, but not NHE3, when Li+ was added to cells at a concentration high enough to saturate their external transport sites as predicted from Li+ affinities. Li+ did not induce phosphatidylinositol (PI) turnover or intracellular Ca2+ mobilization. Li+-induced alkalinization was not affected by protein kinase C down-regulation, loss of glycogen synthase kinase 3beta caused by antisense oligonucleotide treatment, or pretreatment with calphostin C, pertussis toxin, MEK inhibitor PD98059 and PI3-kinase inhibitor LY294002. However, it was markedly suppressed by the tyrosine kinase inhibitor genistein (10 microM). Thus, externally added Li+ activates NHE1 and NHE2 via a mechanism possibly involving a tyrosine kinase, causing an increase in cytoplasmic pH that could potentially affect various cell functions.

Alkalies↗
PubMed2004

Nicotinic receptors and cognition in Parkinson's Disease: the importance of neuronal synchrony.

Parkinson's Disease (PD) is associated with cognitive deficits. The earliest impairment is evident for executive abilities, visuospatial orientation and memory. Dopamine deficiency is unlikely to be singly responsible for all cognitive changes in PD. Acetyl-choline has an essential role in cognition, thus cholinergic transmission may have an important role in non-dopaminergic cognitive changes. If so, some cognitive defects could possibly be treated with choline-esterase inhibitors. A concern is the potential negative motor effect of cholinergic medication in PD. Surprisingly, these are reported only in a few patients studied. Establishing the relationship between select cognitive deficits and nicotinic neurotransmission may lay the foundation for rational pharmacotherapy of cognitive dysfunction in PD. We summarize anatomical, physiological and pharmacological aspects of nicotinic receptor function. The focus is on those nicotine receptor dependent cognitive dysfunctions which are likely to contribute to motor impairment. Lastly, we discuss hypotheses concerning cholinergic involvement in neuronal synchrony and sensorimotor integration in PD.

Cholinergic Agents↗
PubMed1999

P75 nerve growth factor receptor is important for retrograde transport of neurotrophins in adult cholinergic basal forebrain neurons.

The role of the p75 nerve growth factor receptor in the retrograde transport of neurotrophins in the adult CNS was investigated by comparing the transport of 125I-labeled neurotrophins by normal and p75 nerve growth factor receptor-deficient cholinergic septohippocampal neurons. In control mice, nerve growth factor was selectively transported from the hippocampal formation to the cholinergic neurons in the septum. Nerve growth factor labeling was found in three to four times as many septal cholinergic neuronal cell bodies than labeling for neurotrophin-3 or neurotrophin-4/5, and transported brain-derived neurotrophic factor was barely detectable. Cells were considered as labeled when the number of grains per cell exceeded five times background. In p75 nerve growth factor receptor-deficient mice, the number of cholinergic neurons labeled with each of the neurotrophins was reduced by 85-95%. Retrograde labeling of septohippocampal neurons with Fluorogold was not obviously reduced in p75 nerve growth factor receptor-deficient mice, suggesting that general transport mechanisms were not impaired. Despite the reduced neurotrophin transport, cholinergic neurons of p75 nerve growth factor receptor-deficient mice were larger than controls and had an apparently normal density of immunostaining for choline acetyltransferase. Since nerve growth factor is reportedly involved in size regulation and choline acetyltransferase expression, this raises the possibility that the retrograde transport itself is not essential for these events. Thus, p75 nerve growth factor receptor plays an important, although not exclusive, role in the transport of neurotrophins by cholinergic basal forebrain neurons, and retrograde transport of nerve growth factor may not be needed for regulating certain cellular processes.

Animals↗
PubMed1983

Metabolic effects of nicotinamide administration in rats.

Male rats fed a 12% casein diet without choline were injected i.p. daily for 2 or 5 weeks with either saline or 6, 20 or 60 mg of nicotinamide (NAM) per 100 g body weight. Weight gain, food intake and gain/food were lower for the NAM-treated groups compared to the controls. Urinary excretion of the major metabolite, N1-methylnicotinamide (NMN) increased with increasing dose of NAM. NAM administration did not alter the activity of hepatic nicotinamide methyltransferase. Excretion of another metabolite, N1-methyl-2-pyridone-5-carboxamide (2-PYR) was low and showed minimal changes in response to NAM administration. NAM administration did not affect urinary creatinine excretion. Livers of the NAM-injected groups were hypertrophied, and the total lipid content was increased. Kidney hypertrophy was also noted. Plasma and liver choline levels were decreased in response to NAM administration. We conclude that chronic NAM administration resulted in a methyl-group deficiency state due to the greatly increased need for methylation of NAM.

Animals↗