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PubMed1997

Shedding of gangliosides by human medulloblastoma cells.

Shedding of immunosuppressive gangliosides is an important characteristic of both experimental and human tumors. Using a medulloblastoma cell line, Daoy, with a very high ganglioside expression (141 +/- 13 nmol/10(8) cells) and a well-characterized ganglioside complement, we have now studied ganglioside shedding by human brain tumor cells. Shedding of gangliosides, quantified by metabolic radiolabeling, was significant (169 pmol/10(8) cells/h) and was generalized with respect to the major ganglioside carbohydrate structures (G(M2), G(M3), and G(D1a)). For each ganglioside, however, shedding was selective for ceramide structures containing shorter fatty acyl chains. Rapid and ceramide-selective shedding was confirmed in two additional human medulloblastoma cell lines, D341 Med and D283 Med (112 and 59 pmol/10(8) cells/h). Significant ganglioside shedding is therefore a common characteristic of human medulloblastoma cells and may influence the biological behavior of this tumor, in view of immunosuppressive and other biological properties of shed gangliosides.

Cell Division↗
PubMed1997

Neurite outgrowth is enhanced by anti-idiotypic monoclonal antibodies to the ganglioside GM1.

Exogenously added gangliosides enhance sprouting, neurite outgrowth, and other neuronal activities; this effect may be initiated when a ganglioside binds to a membrane protein or when a ganglioside intercalates into the plasma membrane. To test whether binding to membrane proteins is sufficient for ganglioside-mediated activity, anti-idiotypic antibodies were generated that mimic the functional binding sites of the ganglioside GM1 as described by M. J. Riggott and W. D. Matthew (1996, Glycobiology, 6, 581-589). These anti-idiotypic antibodies are proteinaceous probes that model the biochemical and biological effects of gangliosides. Those anti-idiotypic ganglioside (AIG) monoclonal antibodies (mAb's) were selected based on their ability to bind a known GM1 binding protein, the beta-subunit of cholera toxin. These studies described neuronal cell surface proteins that were identified by immunocytochemistry and Western blotting using these AIG mAb's. Here we show that AIG mAb's mimic the functional properties of GM1 in that they facilitate neurite outgrowth from central and peripheral nervous system neurons in in vitro bioassays. In addition, AIG mAb binding modulates second messenger activity, suggesting that membrane protein binding alone is sufficient to invoke intracellular activation. The similarity in the pattern of protein tyrosine phosphorylation evoked by GM1 and the anti-idiotypic ganglioside antibodies suggests that the AIG mAb's modulate neurite outgrowth in a manner similar to that of GM1. Because antibodies cannot intercalate into the plasma membrane, these results suggest that the ganglioside GM1 can mediate neuronal cellular activity by binding to cell surface proteins.

Animals↗
PubMed1988

New trends in ganglioside chemistry.

New methods have been developed for the preparation of highly purified gangliosides, homogeneous in the saccharide, long chain base, and fatty acid moieties and gangliosides carrying different kinds of labelled probes. Gangliosides, homogeneous in the oligosaccharide portion, were prepared by preparative normal phase HPLC on a Lichrosorb-NH-2 column, using a gradient of acetonitrile-phosphate buffer, pH 5.6, as solvent system. Each class of ganglioside (from monosialo- to tetrasialogangliosides) was then submitted to reversed phase HPLC on a preparative RP-8 column, using acetonitrile-5 mM phosphate buffer, pH 7, as solvent system, to obtain gangliosides homogeneous in the long chain base moiety. Gangliosides containing C18 and C20 sphinganine were prepared by catalytic hydrogenation of the corresponding unsaturated gangliosides. GM1 with homogeneous acyl chain was prepared by alkaline hydrolysis in the presence of tetramethylammonium hydroxide (which forms a GM1 deacetylated at the level of sialic acid, and a GM1 deacetylated at the level of sialic acid and deacylated at the level ceramide), followed by re-N-acylation, carried out in the presence of dimethylaminopropyl, ethylcarbodiimide and natural fatty acids, or of mixed anhydride of ethylchloroformate and 14C-stearic acid, and re-N-acetylation performed with acetic anhydride or labelled acetic anhydride. The GM1 derivative, de-acetylated at the level of sialic acid, also produced by alkaline treatment of GM1, was submitted to re-N-acetylation with 14C-acetic anhydride to produce specifically 14C-labelled GM1. Re-N-acylation was carried out a) in the presence of dimethylaminopropyl, ethylcarbodiimide and natural fatty acids, b) with mixed anhydride of ethylchloroformate and 14C-stearic acid. After re-N-acylations, re-N-acetylation was performed with acetic anhydride or labelled acetic anhydride. Gangliosides tritium labelled in the oligosaccharide moiety were prepared by the galactose oxidase/3H NaBH4 method, and gangliosides tritium labelled at carbon-3 of unsaturated long chain bases by the dicyano-dichlorobenzoquinone (DDQ)/3H NaBH4 method.

Animals↗
PubMed1984

Modulatory effects of different temperatures and Ca2+ concentrations on gangliosides and phospholipids in monolayers at air/water interfaces and their possible functional role.

Gangliosides are neuraminic acid-containing glycolipids preferently localized in nervous membranes and showing physicochemical peculiarities, e.g., drastically changing amphiphilic properties by Ca2+ binding. On account of this they are favorite compounds to act as modulators of membraneous organization and functions during synaptic transmission. Lipid monolayers are suitable experimental systems for the study of the surface behavior of amphipatic molecules and therefore are useful to interpret membraneous organization. The surface pressure/area isotherms of monolayers of different individual gangliosides (GM1, GD1a, GD1b, GT1b) of an artificial reconstituted and a natural ganglioside mixture from bovine brain and of ganglioside mixtures from different brain parts of summer- and winter-adapted dsungarian hamsters were compared at three temperatures (11, 20, and 37 degrees C) with egg phosphatidylcholine (PC) and phosphatidylserine (PS) monolayers. The monolayers were formed in a Teflon trough on a triethanolamine/HCl-buffered (pH 7.4) subphase, in some cases containing different amounts of CaCl2. The surface pressure/area isotherms of ganglioside monolayers, in contrast to phospholipids, generally showed slowly rising slopes, with transitions from the liquid-expanded to the liquid-condensed state at a surface pressure of 20-30 mN/m. Ganglioside monolayers, in particular from GD1a or GT1b versus GD1b or from mixtures from summer- versus winter-adapted hamster brain, were differently affected by temperature and/or by Ca2+. PS monolayers were slightly condensed only by Ca2+. PC monolayers, however, were influenced neither by temperature nor by Ca2+. In mixed monolayers of the unpolar natural lipid cholesterol (Ch) and the disialoganglioside GD1a, intermolecular interactions were indicated. Ganglioside monolayers, in contrast to phospholipids, were shown to be easily modulated by temperature and/or Ca2+ ions, thus enabling gangliosides to act as possible membrane modulators, e.g., during synaptic transmission. In particular, the differences concerning the influences of temperature and/or Ca2+ on the surface behavior of ganglioside mixtures from the brain of summer- compared with winter-adapted hamsters are correlated with other physiologically relevant data.

Air↗
PubMed1994

Inhibition of immune cell proliferation and cytokine production by lipoprotein-bound gangliosides.

We have analyzed the immunomodulatory effect of human melanoma gangliosides bound to serum lipoprotein fractions on normal human immune-competent cells in vitro. Total melanoma gangliosides in micelles inhibited proliferation of peripheral blood mononuclear cells stimulated by various mitogens, modulated lymphocyte surface molecules CD2, CD3, CD4, CD5 and CD8 and inhibited the production of interleukin-1 beta (IL-1 beta), tumor necrosis factor alpha (TNF alpha) and IL-6 by stimulated adherent cells. Most of these effects were abrogated in the presence of serum. Purified serum lipoprotein fractions were tested for their ability to allow or inhibit the immunomodulatory effects of gangliosides. Melanoma gangliosides bound to very-low-density lipoproteins (VLDL) were shown to be as potent modulators of the immune response in vitro as when they were presented to cells in the form of micelles. Gangliosides bound to low-density lipoproteins were less active and gangliosides bound to high-density lipoproteins or the lipoprotein-free fraction had no immunomodulatory effects. Given the fact that gangliosides are predominantly bound to lipoproteins in serum, we conclude that lipoproteins are important determinants of the immunomodulating potential of tumor gangliosides, and that the immunomodulatory effects of melanoma gangliosides observed in vitro may also occur in vivo.

Antigens, CD↗
PubMed1998

Ganglioside composition of a mouse brain tumor grown in the severe combined immunodeficiency (SCID) mouse.

The content and composition of gangliosides were examined in an experimental mouse brain tumor, EPEN, that was grown subcutaneously in the flank of the syngeneic C57BL/6J (B6) host and in the B6 severe combined immunodeficiency (SCID) host. SCID mice lack functional T- and B-lymphocytes, but have a normal complement of macrophages. The content and distribution of the brain tumor gangliosides were similar whether the tumor was grown in the immunocompetent B6 host or in the B6-SCID host. N-acetylneuraminic acid- (NeuAc) containing GM3 was the major ganglioside in the subcutaneous tumors and in the cultured EPEN cells. Significant amounts of N-glycolylneuraminic acid- (NeuGc) containing gangliosides were found in the tumor grown in both mouse hosts. NeuGc-containing gangliosides are not expressed in normal mouse brain, but are present in macrophages and serum. An extremely complex pattern of minor gangliosides was found in the subcutaneous tumors on two-dimensional, high-performance thin-layer chromatograms. Most of the minor gangliosides comigrated with those found in mouse macrophages. The results show that the absence of functional T- and B-lymphocytes does not markedly affect brain tumor ganglioside composition and suggest that NeuGc-containing gangliosides in the EPEN can be derived from tumor infiltrating host cells (mostly macrophages) and from the extracellular milieu (serum).

Animals↗
PubMed1984

Gangliosides mediate association of tetanus toxin with neural cells in culture.

Somatic neurohybrid SB21B1 cells grown in serum exhibit limited capacity to bind 125I-labeled tetanus toxin and cannot synthesize gangliosides higher than GM2. By 6 h after supplementing the culture medium with pure or mixtures of brain gangliosides, binding of 125I-labeled tetanus toxin to cells increases approximately 8-fold compared to that of nonsupplemented cells. The uptake of added gangliosides is a saturable process and is facilitated by serum removal (2.1-fold) or substitution of growth factors for serum (3.8-fold). Enhancement of tetanus toxin binding to cells depends on the ganglioside species and concentration; GT1b (25 micrograms/ml) is, respectively, two and three times as effective as GD1b and GM1 in increasing toxin binding. Reconstitution of ganglioside-mediated tetanus toxin binding activity is a reversible phenomenon; removal of medium gangliosides causes a 3-fold drop in toxin binding by 24 h, after which an apparent plateau for at least 3 days above the basal level is established. As in cerebral cultures, binding of toxin to ganglioside-supplemented neurohybrid cells exhibits salt and sialidase sensitivity and is enhanced 2.6-fold at 37 degrees C compared to 0-4 degrees C. The resultant temperature-dependent toxin-cell association is sialidase insensitive. Fixation of cells by formaldehyde or treatment of ganglioside-supplemented cells with trypsin has no substantial effect on ganglioside-mediated binding of the toxin. Methanol/chloroform treatment of cells causes a 91.4% loss of binding activity.

Animals↗
PubMed1992

Generation of murine monoclonal antibodies specific for N-glycolylneuraminic acid-containing gangliosides.

We generated two murine monoclonal antibodies (MAbs) specific for mono- and disialylgangliosides having N-glycolylneuraminic acid (NeuGc) as their sialic acid moiety, respectively, by immunizing C3H/HeN mice with these purified gangliosides adsorbed to Salmonella minnesota followed by fusion with mouse myeloma cells. By use of a wide variety of glycolipids, including NeuGc-containing gangliosides, the precise structures recognized by these two antibodies were elucidated through enzyme-linked immunosorbent assay and immunostaining on thin-layer chromatography. One MAb, GMR8, which was generated by immunizing the mice with purified GM3(NeuGc), reacted specifically with gangliosides having NeuGc alpha 2----3Gal- terminal structures, such as GM3(NeuGc), IV3NeuGc alpha-Gg4Cer, IV3NeuGc alpha-nLc4Cer, V3NeuGc alpha-Gb5Cer, and GD1a(NeuGc, NeuGc). None of the other gangliosides having internal NeuGc alpha2----3Gal- sequences, such as GM2(NeuGc) and GM1(NeuGc), nor corresponding gangliosides having NeuAc alpha 2----3Gal- sequences, nor neutral glycolipids were recognized. Thus, the epitope structures recognized by the MAb were found to be strictly NeuGc alpha 2----3Gal- terminal structures. In contrast, the other MAb, GMR3, which was generated by immunizing the mice with purified GD3(NeuGc-NeuGc-) adsorbed to the bacteria, reacted specifically with gangliosides having NeuGc alpha 2----8NeuGc alpha 2----3Gal- terminal sequences, such as GD3(NeuGc-NeuGc-), IV3NeuGc alpha 2-Gg4Cer, IV3NeuGc alpha 2-nLc4Cer, and V3NeuGc alpha 2-Gb5Cer, but did not react with corresponding gangliosides having NeuAc as their sialic acid moiety or with the neutral glycolipids tested. The epitope structures recognized by the MAb were suggested to be NeuGc alpha 2----8NeuGc alpha 2----3Gal- terminal structures. Using these MAbs, we determined the distribution of such gangliosides in the spleen, kidney, and liver of several mice strains. Novel gangliosides reactive with these MAbs were detected in these tissues.

Animals↗
PubMed1984

Receptor ganglioside content of three hosts for Sendai virus. MDBK, HeLa, and MDCK cells.

Specific gangliosides GD1a, GT1b and GQ1b isolated from brain have been shown to function as receptors for Sendai virus by conferring susceptibility to infection when they are incorporated into receptor-deficient cells (Markwell, M.A.K., Svennerholm, L. and Paulson, J.C. (1981) Proc. Natl. Acad. Sci. USA 78, 5406-5410). The endogenous gangliosides of three commonly used hosts for Sendai virus: MDBK, HeLa, and MDCK cells were analyzed to determine the amount and type of receptor gangliosides present. In all three cell lines, GM3 was the major ganglioside component. The presence of GM1, GD1a and the more complex homologs of the gangliotetraose series was also established. In cell lines derived from normal tissue, MDBK and MDCK cells, gangliosides contributed 47-65% of the total sialic acid. In HeLa cells, gangliosides contributed substantially less (17% of the total sialic acid). The ganglioside content of each cell line was shown not to be immutable but instead to depend on the state of differentiation, passage number, and surface the cells were grown on. Thus, the ganglioside concentration of undifferentiated MDCK cells was found to be substantially greater than that of MDBK or HeLa cells, but decreased as the MDCK cells underwent differentiation. Changes in culture conditions that were shown to decrease the receptor ganglioside content of the cells resulted in a corresponding decrease in susceptibility to infection. The endogenous oligosialogangliosides present in susceptible host cells were shown to function as receptors for Sendai virus.

Animals↗
PubMed1990

Gangliosides in lesion-induced synaptogenesis: studies in the hippocampus of the rat brain.

Changes in ganglioside composition, biosynthesis and individual distribution were studied in hippocampal regions after unilateral destruction of the entorhinal cortex. After 1 and 3 days postlesion (dpl), a decrease in ganglioside content was detected in area dentata (AD) and pyramidal cell regions CA1-CA3 (CA), both ipsilateral and contralateral to the lesion. By 5 dpl all the values had returned to control values, except in AD which showed a dramatic increase in total ganglioside content reaching a maximum at 12 dpl. By 30 dpl this area also showed control content. A significant increase in biosynthesis of gangliosides was observed at 5 and 8 dpl in the hippocampus ipsilateral to the lesion without changes in the contralateral counterpart. Individual ganglioside distribution showed a pronounced change in GM1 and GQ1b with small changes in the other major gangliosides. Significant differences were observed in the distribution of gangliosides between the two hippocampal regions studied in unoperated control animals. GD1a was more concentrated in AD, whereas GQ1b, GT1b and GD1b predominated in CA. The data presented here indicate that important modifications in ganglioside content as well as pattern occur in the deafferented hippocampus a phenomenon that could be related with the known effect of gangliosides on neuritogenesis observed in cell culture studies.

Animals↗
PubMed1996

Immunocytochemical analysis of gangliosides in rat primary cerebellar cultures using specific monoclonal antibodies.

We studied the expression of ganglioside antigens in primary cultures of rat cerebellum using an immunocytochemical technique with mouse monoclonal antibodies (MAbs) specific for various gangliosides. Twelve MAbs that specifically recognize each ganglioside were used. Our study revealed that there is a cell type-specific expression of ganglioside antigens in the primary cultures. A number of b-series gangliosides were detected in the granule cells, whereas a-series gangliosides were not intensely expressed. GD1b was detected in the granule cells. GD2 appeared to be present in a subset of the granule cells or a type of small neurons. GD3 was associated not only with the granule cells, but also with both astrocytes and oligodendrocytes. An O-Ac-disialoganglioside, which was suggested to be O-Ac-LD1, was restrictedly detected in Purkinje cells. The other gangliosides were not detected clearly in these cells. These results suggest that several gangliosides may be useful markers for identifying cells in primary cultures of the rat cerebellum; particularly b-series gangliosides such as GD2 and GD1b for the granule cells and O-Ac-LD1 for Purkinje cells.

Animals↗
PubMed1985

Gangliosides inhibit phenotypic and functional properties of an encephalitogenic T-helper lymphocyte line.

Gangliosides were evaluated for their ability to inhibit the phenotype and function of an encephalitogenic T-helper lymphocyte line from Lewis rats (BP-1), which responds specifically to guinea pig myelin basic protein (GP-BP). After activation for 3 days with GP-BP, the BP-1 line induced a lethal form of experimental autoimmune encephalomyelitis (EAE) in recipient rats 3-6 days after intraperitoneal injection. Incubation of activated BP-1 line cells with 250 microM gangliosides for 1 hr prior to injection prevented EAE completely in 5/14 recipients and markedly reduced the severity of clinical signs and histologic lesions in the rest. Similar treatment of BP-1 cells with galactocerebroside had no inhibitory effect. Both individual and mixed gangliosides inhibited accessory cell-dependent activation of BP-1 cells with GP-BP. Gangliosides also inhibited BP-1 activation with a cell-free supernatant containing accessory cell-processed GP-BP and rat Ia molecules, suggesting that the inhibition was not restricted to accessory cell function. In addition to inhibiting antigen-dependent proliferation, gangliosides inhibited IL-2 dependent cell growth. Furthermore, individual and mixed gangliosides blocked binding of anti-T-helper cell antibody (W3/25) to the BP-1 line, while galactocerebroside, ceramide, and sialic acid had no inhibitory effect. Cell surface staining of T-total, T-non-helper, or Ia determinants was relatively unaffected by gangliosides. Taken together, the immunomodulatory properties of gangliosides on T-effector cell function lend biologic importance to the increased levels of gangliosides which have been reported in human diseases with immunoregulatory abnormalities such as multiple sclerosis, rheumatoid arthritis, and cancer.

Animals↗
PubMed1987

Studies of the mechanism by which gangliosides inhibit the proliferative response of murine splenocytes to concanavalin A.

Gangliosides are known to inhibit the proliferative response of murine and human lymphocytes to antigens and mitogens in vitro. In this study the response of murine spleen cells to concanavalin A (Con A) was used as a model system. Analysis of the cellular events by flow cytometry revealed that during the first 24 hr of culture the effect of gangliosides on Con A-treated cells was minimal. At 48 hr, however, more of the ganglioside-treated cells were in G0/G1, the cells contained more RNA, and fewer cells were in S phase. These data indicate that gangliosides inhibit the transition of the cells from G0/G1 into the S phase of the cell cycle. Expression of the interleukin 2 (IL-2) receptor, as measured by the binding of a monoclonal antibody to the receptor, was not inhibited by the gangliosides. Binding of 125I-labeled recombinant IL-2 to cells cultured for 48 hr with Con A was inhibited by ganglioside GD1a but not by asialo GM1. Inhibition was much more effective if the gangliosides were preincubated with IL-2 before addition of cells, but no inhibition was observed if the cells were preincubated with gangliosides and the unbound gangliosides were washed out prior to addition of the IL-2. These data suggest that interference with the binding of IL-2 to the high-affinity IL-2 receptor of activated T lymphocytes plays an important role in the inhibition of Con A-induced proliferation.

Animals↗
PubMed1991

Gangliosides of human cerebrospinal fluid in various neurologic diseases.

Simultaneous profile determination and quantification of human cerebrospinal fluid (CSF) gangliosides in various neurologic diseases (n = 71) was examined. Gangliosides were extracted with methanol/chloroform from clinically available amounts of CSF (4-5 ml), then separated and quantified by high-performance thin-layer chromatography (HPTLC) and direct densitometry. Based on chromatographic comparison with standards, the percentage of lipid-bound NeuAc positive fractions in 'normal' CSF samples were: GM1 (II3 NeuAc-GgOse4Cer) (3%); GD3 (II3 NeuAc2-Lac-Cer) (4%); GD1a (IV3 NeuAc, II3 NeuAc-GgOse4 Cer) (15%); X1 (3%); GD1b (II3(NeuAc)2-GgOse4 Cer) (16%); X2 (4%); GT1b (IV3 NeuAc, II3(NeuAc)2-GgOse4-Cer) (40%); and GQ1b (IV3(NeuAc)2, II3(NeuAc)2-GgOse4-Cer (15%). Similarity between CSF and CSF and human cerebellar cortex, particularly in proportion of "b" series gangliosides (GQ1b, GT1b, GD1b), could be observed. A higher proportion of GD1a ganglioside, with decreased GQ1b was found in infancy. The total ganglioside content (mean +/- 2 SD) varied between 645-894 micrograms/l. Significant alterations of the CSF ganglioside profile, with an increase in less polar gangliosides, GM3 and GD3, correlated with the blood-brain barrier dysfunction (CSF hemorrhages, compressive syndrome), or some malignant processes (metastatic brain melanoma). A statistically significant increase in the content of total CSF gangliosides was found in the following groups of patients as compared to controls: (1) ischemic cerebrovascular accident (CVI) with good outcome (P less than 0.02); (2) peripheral neuropathy and polyneuropathy (P less than 0.001) and (3) intravertebral discopathy (P less than 0.05). A significant decrease in the content of total CSF gangliosides was found in CVI group with lethal outcome (P less than 0.05).

Adult↗
PubMed1985

Gangliosides in postmitotic retina of chick embryo: changes in vivo and in cell cultures.

Developmental changes in ganglioside composition of postmitotic neural retina of chick embryo were analyzed by thin-layer chromatography. Gangliosides were identified by comparing their chromatographic mobilities with reference standards. The outstanding changes are decrease in the concentration of GD3L and increase in GD1a and GM1 concentrations. By depleting Müller glia cells from retina tissue of 13- and 16-day embryos (R13, R16) we determined that the bulk of the major gangliosides is associated with the neurons. Analysis of gangliosides in monolayer cultures of R13 and R16 cells highly enriched for Müller cell-derived gliocytes indicated that these cells express the same types of gangliosides as neurons, but in somewhat different concentrations and relative proportions; however, after time in culture these cells showed ganglioside types and changes in ganglioside profile that are not characteristic of normal retina. The latter observation is consistent with other evidence that the phenotype of Müller glia cells becomes altered in monolayer culture. In contrast to cultures of early embryonic retina, in organ cultures of later postmitotic retina, ganglioside composition did not continue to change as in normal development. This suggests that in postmitotic retina, normal developmental progression of ganglioside changes requires systemic and/or other conditions which are missing or altered when this tissue is isolated and cultured in vitro.

2-Aminoadipic Acid↗
PubMed1991

Altered biosynthesis of gangliosides in developing biliary cirrhosis in the rat.

The biosynthesis of gangliosides was studied in developing biliary cirrhosis in rats 14, 28, and 42 days after bile duct obstruction. The total content and patterns of gangliosides in livers and sera, and the activity of six hepatic ganglioside synthases in a cell-free system were determined. Up to 7-fold increased synthase activities were strictly correlated in time and extent with increased total contents of gangliosides in liver and serum. In addition, altered patterns of serum gangliosides were observed. The results clearly demonstrate that the liver is the main source of elevated serum gangliosides in biliary cirrhosis in the rat. Increased hepatic biosynthesis and the secretion of gangliosides into the serum appear to be an important pathogenetic event. Alterations of hepatic enzyme activities indicate that GL2 and GM3 synthase regulate total hepatic ganglioside content. However, certain abnormalities in ganglioside patterns which were observed in the liver and sera of cirrhotic animals can not be explained by changes in hepatic enzyme activity. They indicate additional pathobiochemical mechanisms to be involved, e.g., altered hepatocellular processing and/or impaired secretion into bile.

Animals↗
PubMed1992

Gangliosides in the human brain development and aging.

In this study, brain gangliosides in prenatal and postnatal human life were analyzed. Immunohistochemically, the presence of "c"-pathway of gangliosides (GQ1c) in embryonic brain was only recorded at 5 weeks of gestation. Biochemical results indicated a twofold increase in human cortex ganglioside concentration between 16 and 22 weeks of gestation. The increasing ganglioside concentration was based on an increasing GD1a ganglioside fraction in all regions analyzed except cerebellar cortex, which was characterized by increasing GT1b. In this developmental period, GD3 was found to be localized in the ventricular zone of the cortical wall. After birth, GD1b ganglioside in neuropil of granular cell layer corresponding to growing mossy fibers was expressed in cerebellar cortex. Between birth and 20/30 years of age, a cerebral neocortical difference of ganglioside composition was observed, characterized by lowest GD1a in visual cortex. Analyzing the composition of gangliosides in cortical regions during aging, they were observed to follow region-specific alterations. In frontal cortex, there was a greater decrease in GD1a and GM1 than in GT1b and GD1b, but in occipital (visual) cortex there was no change in individual gangliosides. In hippocampus, GD1a moderately decreased, whereas other fractions were stable. In cerebellar cortex, GD1b and GT1b fractions decreased with aging.

Abortion, Legal↗
PubMed1984

Brain gangliosides in hibernating dormice (Glis glis) and cold-exposed laboratory mice.

The concentration of proteins, sialo-glycoproteins and gangliosides and the ganglioside composition of 8 brain regions from normothermic and hibernating fat dormice (Glis glis) and from laboratory mice being acclimated to 6, 22 and 28 degrees C were investigated. During hibernation the concentration of sialo-glycoproteins and gangliosides decreased significantly in brain of dormice; the protein content remained uninfluenced. Cold-exposure of laboratory mice yielded generally a slightly decreased sialo-glycoprotein concentration in brain; the data on ganglioside concentration in the CNS were not uniform. The ganglioside composition of brain of laboratory mice being kept at different environmental temperatures did not show any alterations. The brain gangliosides of hibernating dormice in contrast to their normothermic counterparts are more polar (higher amount of GTlb and GQlb.). Most striking is the complete absence of a distinct ganglioside fraction (O-acetylated-GTlb) during hibernation. Brain gangliosides of normothermic dormice were found to be more sensitive against neuraminidase treatment than those of hibernating animals. The results are discussed with regard to modulatory functions of neuronal gangliosides for the process of synaptic transmission during seasonal adaptation.

Animals↗