Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “GANGLIOSIDES”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,243 records · Page 69Linked to original sources
PubMed1985

Effect of neonatal thiamine and vitamin A deficiency on rat brain gangliosides.

Effects of neonatal thiamine deficiency and vitamin A deficiency on total and fractions of gangliosides (GT1, GD1a, GD1b and GM1) were studied in Charles Foster rat brain at 21 days of age. GT1, GD1b+GD1a and GM1 are being presented here as poly-, di- and mono-sialo gangliosides. Thiamine and vitamin A deficiencies were induced by feeding mothers essentially thiamine and vitamin A free diets respectively. A normal control (G+L+) and weight matched undernourished groups (G+L- for thiamine and LL for vitamin A experiments) were used for comparison. At 21 days, the concentration of total gangliosides in thiamine deficient and G+L- rat brains were 49.0% and 45.7%; in vitamin A deficient and LL group were 66.6% and 88.0% of the G+L+ group, respectively. The percent contribution of poly-, di- and mono-sialo gangliosides in G+L+/thiamine deficient/G+L- were; 17.2/46.8/73.5, 54.4/51.7/14.2, and 6.6/8.7/5.8, respectively. The percent contribution of poly-, di- and mono-sialo gangliosides in G+L+/vitamin A deficient/LL were; 19.3/39.9/43.7, 57.0/37.6/35.1, and 8.4/11.6/19.7 respectively. The changes observed in these experiments suggest an underlying possibility of metabolic defect in undernourished animals.

Animals↗
PubMed1995

Inhibition by gangliosides GM3, GD3 and GT1b of substrate phosphorylation by protein kinase C in bovine mammary gland and its reversal by phosphatidylserine.

Effects of gangliosides GM3, GD3 and GT1b on protein kinase C (PKC) activity and endogenous protein phosphorylation by PKC were examined in bovine mammary gland. The gangliosides inhibited PKC activity in both cytosolic and total particulate fractions with IC50 values (concentrations causing 50% inhibition) of 100-115 microM (GM3), 75-80 microM (GD3) and 20-28 microM (GT1b). Several proteins were shown to be substrates for PKC by phosphorylation in the absence or presence of the PKC cofactors 1-oleoyl-2-acetyl-sn-glycerol (OAG, 5 micrograms/ml), phosphatidylserine (PS, 25 micrograms/ml) and Ca2+ (1 microM). GM3 at 100 microM suppressed phosphorylation in cytosol of 91 kDa and 89 kDa proteins. Similar suppression of phosphorylation of these proteins was achieved by the addition of 50 microM GD3 and 10 microM GT1b; thus the order of suppressive capacity for substrate phosphorylation was parallel to their IC50 values. GT1b (100 microM) inhibited phosphorylation of 56 kDa, 43 kDa and 36 kDa proteins, in addition to that of the 91 kDa and 89 kDa ones. Phosphorylation of 72 kDa and 21 kDa proteins was resistant even at this concentration, suggesting the selective suppression by gangliosides of phosphorylation of individual substrates. In the particulate fraction, phosphorylation of a 91 kDa protein was suppressed by 100 microM GT1b, whereas phosphorylation of the other substrates was unaffected by any ganglioside used. Suppression of phosphorylation of cytosolic 91 kDa and 89 kDa and particulate 91 kDa proteins could be reversed by addition of PS (250 micrograms/ml), but not by OAG (50 micrograms/ml) or Ca2+ (250 microM). These results suggest that gangliosides are involved in the regulation of PKC-dependent phosphorylation by modulating the association of PKC or its substrates with membrane phospholipids.

Animals↗
PubMed1995

Gangliosides raise the intracellular Ca2+ level in different cell types.

Total gangliosides from bovine brain at micromolar concentration induce intracellular Ca2+ increments in a temperature, time and dose dependent manner when assayed with suspensions of rat macrophages, rat and chicken neurons, human erythrocytes and liposomes, loaded with the fluorescent Ca2+ indicator FURA 2. The effect was independent on the endogenous ganglioside composition of the cells and in the case of neurons it was also independent on the differentiation state. Gangliosides do not induce the release of Ca2+ from inner stores. These findings indicate that the reported inhibition of arachidonic acid release (Bressler, J., et al., (1994) Life Sci., 54, 49-60) and anti-inflammatory properties of gangliosides (Correa, S.G. et al., (1991) Eur. J. Pharmacol. 199, 93-98) are not due to impairments of Ca2+ flux. The results also suggest the possibility that the well-known neurotrophic effect produced by gangliosides on undifferentiated neurons in culture may be due to subtoxic cytosolic Ca2+ increments.

Animals↗
PubMed1989

Behavioural and morphological changes following treatment with GM-1 ganglioside of rats with an electrolytic lesion of the substantia nigra.

The effects of daily treatment with GM-1 ganglioside (30 mg/kg i.p.) or saline (1 ml/kg i.p.) in rats with discrete unilateral electrolytic lesions of the dorsal substantia nigra were investigated. Treatment with GM-1 ganglioside, beginning 3 days prior to surgery and continuing for 33 days post-operatively, caused reductions in the total ipsilateral turns and peak turning rates induced by apomorphine (0.75 mg/kg s.c.) between 7 and 31 days post-operatively, without altering the time course of the effect of apomorphine. No effects of GM-1 on lesion-induced changes in synaptosomal uptake of [3H]dopamine, dopamine, serotonin in the striatum or corresponding levels of metabolites were found. Treatment with GM-1 ganglioside had no effect on the rostrocaudal extent of the electrolytic lesion, but caused morphological changes at the site of the lesion, including a reduction in the density of glial cells. Treatment with GM-1 ganglioside resulted in a relative preservation of cell bodies, staining immunocytochemically for tyrosine hydroxylase, in the substantia nigra pars compacta (expressed as a percentage of the intact side), when compared with saline-treated rats. The results showed that GM-1 ganglioside promoted a partial functional recovery from apomorphine-induced circling, which may be due in part to a reduction in the extent of damage at the lesion site.

Animals↗
PubMedDate not supplied

Brain gangliosides: increased incorporation of (1- 3H) glucosamine during training.

The incorporation of (1-3H)glucosamine into biochemical fractions of brain was studied in mice trained in a conditioned avoidance jump-up task, in mice yoked to the trained animals, and in undisturbed mice in their home cages. The (3H)glucosamine was injected subcutaneously 15 min before 15 min of training, and the mice killed after a total pulse time of one hour. There was a consistent and significant increase of about 21 percent of the incorporation of the 3H into the brain ganglioside fraction when trained mice were compared with quiet mice. This increase was not observed in any of the other chemical fractions studied, including the total chloroform-methanol-soluble compounds, the non-ganglioside lipids, and the chloroform-methanol-insoluble compounds (radioactivity principally in glycoprotein). Yoked mice showed an intermediate level of incorporation, exhibiting only a 12 percent increase in the ganglioside fraction. When the individual ganglioside species were analyzed by thin-layer chromatography the changed incorporation was not specific for any ganglioside species.

Animals↗
PubMed1983

Ganglioside treatment of alcoholic neuropathies: experimental and clinical aspects.

Recent research results indicate that gangliosides, complex glycolipids present in neuronal membranes, play an important functional role in nervous transmission. Physiological and pharmacological investigations have shown that the parenteral administration of a bovine cerebral cortex ganglioside preparation exerts a reinnervation-stimulating activity, due to enhanced nerve sprouting, in peripheral neuropathies. Experimental data are presented showing that the administration of ganglioside prevents the decrease of the conduction velocity, measured in the sciatic nerve of laboratory animals chronically intoxicated with ethanol. Gangliosides are also able to improve the conduction velocity in the sciatic nerve of animals already damaged by the same neurotoxic agent. With regard to therapeutical aspects in alcoholic patients with sensory or motor-sensory polyneuropathy, a review is presented covering 114 patients studied in several clinical trials by means of clinical and instrumental investigations. The clinical parameters, especially the sensory disturbances, turn out to be very responsive to ganglioside treatment. Also, the electrophysiological effects are positively influenced, even though this kind of investigation presents methodological difficulties connected with the great variability of baseline data.

Alcoholism↗
PubMed1986

Specificity of ganglioside binding to rat macrophages.

The binding specificity of rat alveolar macrophages (AM phi) for sheep erythrocytes (E) coated with gangliosides GM1, GM2, GM3, GD1a, GD1b or GT1b was analyzed in a rosette assay by studying the inhibitory effect of gangliosides, various carbohydrates, IgG, C3b-like C3, and fibronectin in this assay. The uptake of gangliosides by E was calculated from radioactivity measurements using 3H-labeled gangliosides. The different gangliosides were taken up by E at 37 degrees C to a similar extent. Uptake of 3H-labeled GM2 correlated linearly to its concn in the incubation medium. Erythrocytes pretreated with the same molar concn of GM2, GD1a, GD1b or GT1b were bound to AM phi to the same degree reaching a maximum of about 90% rosette forming cells. A mean of 17.8% AM phi-bound GM3-coated E. Treatment of E with asialo-GM2 (GA2) or GM1 did not induce significant rosette formation. A dose-dependent inhibition of rosette formation was observed when AM phi were preincubated at 0 degree C with GM2, GM3, GD1a, GD1b or GT1b, but not with GM1 or GA2 Of the tested carbohydrates, sialyl-lactose had a strong inhibitory effect, while lactose was completely ineffective. N-acetyl-neuraminic acid, N-glycolyl-neuraminic acid and N-acetyl-galactosamine were slightly inhibitory. A series of other carbohydrates including highly negatively charged compounds, as well as fibronectin, IgG or C3b-like C3 did not show significant inhibition. Our data indicate the expression of a receptor on rat AM phi recognizing carbohydrates containing sialic acid at or near the non-reducing terminus.

Animals↗
PubMed1982

Gangliosides and proteins in developing chicken brain myelin.

Ganglioside and protein content of chicken brain myelin have been studied as a function of development and maturation. Ganglioside concentration remained relatively constant at approximately 225-266 micrograms sialic acid per 100 mg myelin, from 17-day-old embryos to 540-day-old adults. The ganglioside distributional pattern was also constant, GM1 and GM4 each accounting for approximately one-third of total sialic acid. These properties are contrasted with those of mouse and rat brain myelin which previously showed enrichment of GM1 at early stages of myelination and appearance of GM4 at a later stage of maturation. In an earlier study of the mouse total myelin gangliosides doubled in concentration between 3 and 5 weeks of age and full maturity. Myelin proteins of the chicken also remained relatively constant in concentration and distributional pattern during development, although the percentage of basic protein increased somewhat during the first few weeks after hatching. Correlations were observed between molar concentrations of basic protein and various gangliosides, particularly the monosialo types.

Aging↗
PubMed1991

Correlation of gangliotetraose gangliosides with neurite forming potential of neuroblastoma cells.

Gangliosides of 11 different neuroblastoma cell lines, grown to confluence, were extracted and quantified with respect to: (a) total lipid-bound sialic acid, (b) total gangliotetraose family, and (c) GM1 content. The cultured cells were induced to grow neurites in 3 ways: (a) serum reduction, (b) exogenous ganglioside, and (c) retinoic acid. Neurite outgrowth was quantified in terms of % of cells bearing neurites and average number of neurites per cell. No correlation was observed between neurite outgrowth and total ganglioside concentration, but a reasonably good correlation was observed with respect to neuritogenesis and gangliotetraose content. When exogenous ganglioside was the stimulant the best correlation was with GM1, whereas retinoic acid-stimulated outgrowth was approximately proportional to GD1a content. The 'neurite minus' N1A-103 line, which had the lowest level of GM1, GD1a, and total gangliotetraose gangliosides, showed little if any response to any of the stimuli.

Animals↗
PubMed1996

Differential expression of gangliosides and galactolipids in fetal human oligodendrocytes and astrocytes in culture.

The phenotypic expression of gangliosides and galactolipids was investigated using primary cultures of fetal human oligodendrocytes and astrocytes. These glial cells were isolated from fetal human brains of 12-18 weeks' gestation. Expression of gangliosides and galactolipids in oligodendrocytes and astrocytes was investigated by double labeling immunocytochemistry using rabbit antibodies specific for galactocerebroside (GalC, a cell type-specific marker for oligodendrocyte) and glial fibrillary acidic protein (GFAP, a cell type-specific marker for astrocyte) in combination with a panel of mouse monoclonal antibodies which react with specific gangliosides or galactolipids. A considerable number of GalC+ oligodendrocytes expressed intense immunoreactivities specific for GM3 (19%) and GM2 (45%) gangliosides. Approximately 11% of GalC+ oligodendrocytes expressed GM4 immunoreactivity, and smaller numbers of GalC+ oligodendrocytes expressed GD3 (4%), GD2 (1%), GT1b (5%) and A2B5 (3%) immunoreactivities. However, GalC+ oligodendrocytes did not express GM1, GD1a, GT1b or GQ1c. Major populations of GalC+ oligodendrocytes immunolabeled by rabbit anti-GalC antibody reacted with anti-GalC mAb (Ranscht mAb, 81%) or by anti-sulfatide mAb (O4 mAb, 91%). A considerable number of GFAP+ astrocytes expressed intense GM2 (26%) and GD2 (15%) immunoreactivities, while a smaller population expressed intense GM3 (3%), GD3 (6%) and GM4 (4%) immunoreactivities. Weak immunoreactions specific for GD1b, A2B5 and sulfatide were found in less than 1% each of GFAP+ astrocytes, while GFAP+ astrocytes did not express GM1, GD1a, GT1a, GT1b or GQ1b. These results indicate that GM3, GM2 and sulfatide are expressed in a major population of GalC+ oligodendrocytes, while GM3, GM2, GD3, GD2, and GM4 are expressed in a small but distinctive population of GFAP+ astrocytes. Our results suggest that GM4, GM1 and GD3, which are utilized as markers for adult human oligodendrocytes and myelin, are not the major ganglioside constituents in cultured fetal human oligodendrocytes.

Antibodies, Monoclonal↗
PubMed1992

Influence of gangliosides on experimental allergic neuritis.

The development of myelin-induced experimental allergic neuritis (EAN) in Lewis rats can be depressed and delayed by adding a ganglioside mixture (GM1, GD1a, GD1b, GT1b) to the immunization compound; however, gangliosides may enhance the induction of adjuvant arthritis. Antibodies against multiple gangliosides are produced in rats after immunization with gangliosides after addition of myelin, but only low titers can be detected in animals immunized with myelin and complete Freund's adjuvant alone. We conclude that this antibody production is not the result of peripheral nerve inflammation but depends rather from external applied gangliosides.

Animals↗
PubMed1993

Effects of ganglioside administration on experimental autoimmune neuritis induced by peripheral nerve myelin or P2-specific T cell lines.

We studied the effects of ganglioside administration in two animal models of inflammatory demyelinating polyneuropathy. We administered a mixture of bovine brain gangliosides intraperitoneally to Lewis rats with myelin-induced or T cell line-mediated experimental autoimmune neuritis (EAN). Under the experimental conditions we had chosen, we only detected marginal but not statistically significant effects on disease course and severity, as evidenced by motor function, electrophysiological findings, and morphological signs of inflammation and demyelination. There was no significant induction of antibody production against gangliosides, and we did not detect signs of increased cellular reactivity towards gangliosides. We conclude that the administration of gangliosides modulates EAN at best marginally, and does not induce a cellular or humoral immune reaction.

Animals↗
PubMed1987

Behavioural recovery from unilateral vestibular lesion is facilitated by GM1 ganglioside treatment.

Exogenously administered gangliosides function in vivo to facilitate survival and repair of damaged neurones in both central and peripheral nervous systems. These effects have been attributed to their neuritogenic and neuronotrophic properties. In this investigation the effects of ganglioside treatment have been studied on the compensation that follows a unilateral labyrinthectomy, considering that the vestibular recovery is supposed to be achieved through a mechanism of sprouting acting on the deafferented neurones. Hemilabyrinthectomized guinea pigs were given a daily injection of either GM1 ganglioside (30 mg/kg, i.p.) or saline for 21 days. As regards postural symptoms, the GM1 group more quickly restored a posture of the head non-deviated in the horizontal plane, while the remaining postural symptomatology was not significantly affected by the treatment. Furthermore, the GM1-treated group attained more rapidly an ocular position characterized by very slow drifts (or by no drift at all), directed towards the side of the intact labyrinth. Ganglioside treatment did not reduce the severity of the initial hemilabyrinthectomy impairments and the effect of the treatment became evident with time. This result is consistent with the hypothesis that also in this model of neuronal plasticity, gangliosides act by enhancing reactive synaptogenesis on the deafferented vestibular neurones.

Afferent Pathways↗
PubMed1992

Study of brain and vascular plexus gangliosides in meningoencephalitis of various etiology.

The content of brain and vascular plexus gangliosides and their composition have been studied in 15 cases of meningoencephalitis of various etiology and degree of disease. The most pronounced decrease of ganglioside concentration was found in brain of children, who died from herpes virus infection. Decrease of ganglioside content was revealed in brain grey matter of patients with influenza virus or meningococcus infection, but not in cases of mycoplasma infection. These data provide evidence of nerve cell destruction due to meningoencephalitis of various etiology. The biochemical data obtained are in good agreement with the results of the brain of children infection by herpes virus (increase of GD1b content in grey matter). Ganglioside content in vascular plexes of patients with meningoencephalitis was found to be, on the contrary, much higher (ca 4 times) than in the controls. The higher the lesion of choroid plexes in meningoencephalitis is, the higher the ganglioside content in them is.

Brain↗
PubMed1979

Creutzfeldt-Jakob disease--alteration in ganglioside sphingosine in the brain of a patient.

Gangliosides isolated from the brain of patients with Creutzfelt-Jakob (C-J) disease were analyzed. The ganglioside current was abnormally low, and the percentage distributions of individual gangliosides and the long-chain base compositions were abnormal. The C20-sphingosine contents of all the ganglioside fractions were low. Abnormalities in ganglioside long-chain bases in adult human brain have been reported previously only in patients with inherited metabolic disorders. These abnormalities in C-J disease seem to be closely related to the cause of the disease.

Brain Chemistry↗
PubMed1980

Interaction between Clostridium botulinum neurotoxin and gangliosides.

The effect of gangliosides on Clostridium botulinum type A neurotoxin was examined in terms of detoxification. The molar concentrations of gangliosides necessary to detoxify 50% of 1 M Cl. botulinum neurotoxin were as follows: GM1, 2073; GM2, 2439; GM3, 6098; GD1a, 610; GD1b, 488; GT1a, 829; GT1b, 6 and GQ1b, 27. Inhibition by gangliosides of the neurotoxin binding to synaptosomes showed that GT1b was highly effective, but the others were not. Low-temperature treatment inhibited the detoxification of neurotoxin by GT1b and the binding of 125I-labelled neurotoxin to the synaptosome fraction. 125I-labelled neurotoxin was mixed with GM1 or GT1b and their molecular size was estimated by sucrose-density-gradient centrifugation. When 125I-labelled neurotoxin was incubated with GM1, a single radioactive peak having a sedimentation coefficient of 7.3 S appeared. When incubated with GT1b, however, 125I-labelled neurotoxin gave three peaks having sedimentation coefficients 14, 10 and 7.3 S, respectively. The present results indicated that the location and the number of sialic acids in ganglioside molecules are of significance in the detoxification and the binding of Cl. botulinum neurotoxin with ganglioside molecules.

Animals↗
PubMed1987

Ganglioside composition of liver and kidney from rat after pentazocine treatment.

1. Female non-pregnant rats were intramuscularly injected with pentazocine for 3 months. Liver showed a statistically significant (P less than 0.05) increase in its ganglioside content after the pentazocine treatment; in addition, no changes were found in the kidney ganglioside content. 2. We have also found changes in the ganglioside pattern of these rats after the pentazocine injection. The GM1 and GD1b liver content was decreased (P less than 0.05) in parallel with an increase (P less than 0.05) in GD3 and GT1b content; kidney showed a decrease (P less than 0.05) in GM1, GD1a and GD1b content and an increase (P less than 0.05) in GM4, GD2, GT1b and GQ content. 3. Female pregnant rats were also injected with pentazocine from the first to the nineteenth day of the gestation period. The total ganglioside content of liver and kidneys from mothers and their newborns did not show statistically significant differences after the treatment. 4. Mothers showed a decrease (P less than 0.05) in the GM1 content of liver and an increase (P less than 0.05) in the GT1b content of liver and GM1, GD3 and GD1a content of kidney. Only the GM3 content from kidney was increased (P less than 0.001). 5. Newborns showed minor changes in their ganglioside pattern. GT1b content from liver and GD2 and GQ content from kidneys were decreased (P less than 0.05).

Animals↗
PubMed1982

The stimulating effect of ganglioside injections on the recovery of choline acetyltransferase and acetylcholinesterase activities in the hippocampus of the rat after septal lesions.

The effect of intramuscular administration of a mixture of gangliosides (21% GM1, 39.7% GD1a, 16% GD1b, 19% GT1) in a daily of 50 mg per kg upon the time course of changes in hippocampal acetylcholinesterase and choline acetyltransferase activities after extensive medioventral septal lesions in the rat was checked on days 3, 5, 18 and 50 after the operation. Following the early decrease in the enzyme activities to about 25% of control due to degeneration, a gradual recovery up to about 50% of control activity at the 50th day was found. When gangliosides were administered, the recovery in the activity of both enzyme was more pronounced. The ratio of the enzyme activities from the animals injected with gangliosides to that from uninjected animals was 1.45 and 1.48 on the 18th day and 1.62 and 1.50 on the 50th day after the operation, for choline acetyltransferase and acetylcholinesterase activity, respectively. Since no significant effect of ganglioside injection was seen at early post-operative times i.e. on days 3 and 5, the effects seen on days 18 and 50 seem to be specifically due to facilitation of the recovery processes and not to retardation of the degeneration processes. Assuming that the spontaneous recovery of cholinergic enzyme activity reflects reinnervation of the hippocampus through collateral sprouting gangliosides would seen to facilitate the regrowth of new cholinergic nerve terminals.

Acetylcholinesterase↗