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PubMed1984

Gangliosides of human spinal cord: aberrant composition of cords from patients with amyotrophic lateral sclerosis.

The ganglioside content of formalin-fixed human spinal cords and fresh human spinal cords was found to be both quantitatively and qualitatively similar. However, the spinal cord was found to be heterogeneous with respect to ganglioside content. In particular, a gradient of GD1a was observed, increasing from a low content in the cervical region to a relatively high content in the sacral region. Comparison of the ganglioside content of nine normal spinal cords and nine spinal cords from clinically diagnosed amyotrophic lateral sclerosis (ALS) patients revealed no major quantitative differences, but the unique presence of three additional gangliosides in ALS spinal cords. One of these was tentatively identified as sialosylglobotetraosylceramide and was absent from eight of nine control spinal cord samples, the sole exception being the cord from a 97-year-old female.

Adult↗
PubMed1985

Ganglioside patterns during cerebral development in the normal and reeler mouse.

Gangliosides were extracted from cerebral tissue of reeler and normal mice, and analyzed by two-dimensional thin-layer chromatography at embryonic and postnatal ages. The ganglioside pattern changed substantially as development proceeded in the telencephalon of both reeler and normal mice, but was the same at any given age for both conditions, despite the marked histological differences between reeler and normal samples. These results indicate that abnormal ganglioside patterns do not result from the reeler mutation at early stages of brain development, and that the cell misalignment characteristic of the reeler phenotype involves molecules other than gangliosides.

Animals↗
PubMed1988

Influence of monensin on ganglioside anabolism and neurite stability in cultured chick neurons.

We have examined the effects of monensin, a monovalent cationophore that disrupts exo- and endocytosis of membrane vesicles and diminishes Golgi anabolic function, on the incorporation of [3H]-galactose into glycosphingolipids in neurited primary cultures of chick embryo central nervous system neurons. A linear rate of incorporation into all ganglioside species from extracellular-labeled galactose was observed. Specific activity of anabolic labeling was markedly lower in GT1b and GQ1b than in the other major gangliosides of the embryonic neuron (GM3, GD3; GM2, GD2; GM1, GD1a, GD1b). With 100 nM monensin in the extracellular medium, the rate of labeling of GT1b diminished markedly to 20% of control; GD1a, GD1b, and GD2, to 35%; GQ1B to 48%; GD3 to 60%. Vigorous incorporation of label into GM3 was entirely undiminished by monensin. From these findings, it is suggested that ganglioside biosynthesis is compartmentalized in the cytodifferentiating embryonic neuron, with GM3 entirely, and GD3 and GQ1b partially, an extra-Golgi product. Extensive loss of neurites that occurred after several hours of exposure of the neurons to monensin could not be correlated directly with decreased ganglioside anabolism.

Animals↗
PubMed1989

EGF-induced neuritogenesis and correlated synthesis of plasma membrane gangliosides in cultured embryonic chick CNS neurons.

Epidermal growth factor (EGF), over a low range of concentrations (165-825 pM), induced neuritogenesis in post-mitotic chick CNS precursor neurons cultured in a serum-free medium, without the addition of other growth factors. Antibody to EGF blocks the neurite-promoting activity of EGF. Similarly, neuritogenesis of cultured chick CNS neurons in medium supplemented with 20% fetal bovine serum is blocked by antibody to EGF, even though serum may contain other neuronotrophic bioactive proteins and steroids. Quantitatively, the only major gangliosides of the undifferentiated post-mitotic neurons are GD3 and GD2. GD3 as well as its biosynthetic precursor, GM3, undergo active biosynthesis in serum-free medium as evidenced by their vigorous labeling by radioactive galactose supplied in the culture medium. When the undifferentiated neurons in serum-free medium are exposed to EGF, the ensuing generation of neurite plasma membrane coincides with initiation of biosynthesis of the sialosyl gangliotetraosyl ceramide species of gangliosides (GD1A, GD1B, GT1B, GQ1B). Antibody to EGF simultaneously inhibits biosynthesis of these gangliosides as well as inhibition of neuritogenesis. These findings indicate that EGF may be a primary neurite-inducing growth factor for post-mitotic embryonic CNS neurons and that gangliosides, particularly those of the sialosyl gangliotetraosyl ceramide species, characterize the plasma membrane of CNS neurons during neuritogenesis.

Animals↗
PubMed1990

Cerebellar ganglioside abnormalities in pcd mutant mice.

The distribution of cerebellar gangliosides was studied in Purkinje cell degeneration (pcd/pcd) mutant mice at postnatal days 25, 30, 50, and 150. These mutants lose the majority of Purkinje cells between 18 and 50 days of age. A reactive gliosis accompanies Purkinje cell loss and a partial loss of granule cells occurs in pcd/pcd mice older than p50. Purkinje cell loss is associated with significant reductions in cerebellar weight and ganglioside concentration. This neuronal loss was also developmentally correlated with reductions of gangliosides (GT1a/LD1 and GT1b and with elevations of GD3. These results agree with previous findings in other cerebellar mutants that GT1a/LD1 and GT1b are concentrated in Purkinje cells and that GD3 is enriched in reactive glial cells. A slight, but significant, reduction in GD1a concentration occurred only in older pcd/pcd mice, consistent with previous findings in weaver and staggerer mice that GD1a is enriched in mature granule cells. The findings with pcd/pcd and other neurological mutants indicate that certain gangliosides can serve as cell-surface markers for monitoring changes in cerebellar cytoarchitecture that accompany development or disease.

Animals↗
PubMed1992

Exogenous gangliosides modulate calcium fluxes in cultured neuronal cells.

Previous work from this and other laboratories has shown that the neuritogenic effect due to exogenous gangliosides on primary neurons in culture is accompanied by several morphological and biochemical modifications. The present results indicate that the treatment of these neurons with gangliosides, under the experimental conditions which are known to produce a sprouting effect, inhibited the influx of 45Ca2+ and increased the release of 45Ca2+ from the cells. No significant differences were noted using concentrations of gangliosides (10(-8)-10(-5) M) either below or above the critical micellar concentrations. No apparent specificity was observed among various species of individual sialocompounds (GM1, GD1a). Moreover the presence or absence of fetal calf serum in the culture medium influenced the levels of 45Ca2+ fluxes. This study confirms the hypothesis that gangliosides may be considered as Ca2+ flux modulators in neuronal cells.

Animals↗
PubMed1982

Gangliosides and sialoglycoproteins in normal and denervated rat diaphragm muscle.

Ganglioside-and glycoprotein-bound sialic acid in endplate and non-endplate regions of rat diaphragm muscles were assessed 1-16 days after phrenic nerve transection. Sialic acid in glycoproteins (90% of total) and gangliosides (10% of total) from intact hemidiaphragms was distributed uniformly throughout endplate and nonendplate regions. Afer denervation, the total sialic acid per hemidiaphragm increased (days 1-4) and reached a maximum level (days 8-12) which remained constant (days 12-16). These sialic acid changes reflected increments in gangliosides (40% over control), which occurred simultaneously in endplate and non-endplate regions (days 1-8), and increments in sialoglycoproteins (70%-80% over control), which took place much earlier in endplate (days 1-8) than in nonendplate (days 8-14) regions. The results of this study, together with previous data, favor the hypothesis that maintenance of both sialoglycoproteins and gangliosides depends upon an intact innervation, probably through separate mechanisms involving different neurogenic factors.

Animals↗
PubMedDate not supplied

Electromyographic study of diabetic and alcoholic polyneuropathic patients treated with gangliosides.

A double-blind, randomized electromyographic investigation was conducted of the effects of cerebral ganglioside treatment on patients suffering from diabetic or alcoholic polyneuropathy. Cerebral gangliosides (50 mg once a day) administered to 15 diabetic and to 15 alcoholic neuropathic patients for 40 days, facilitated the reappearance of sensory potentials and significantly increased the MAP amplitude in median, ulnar, and peroneal nerves. In relation to ganglioside treatment, there was no significant change in the conduction velocities or in the distal latencies of these nerves, nor was there a change in the duration of the MAPs. On the basis of these results, it is suggested that the cerebral gangliosides are capable of inducing an improvement in the excitability of nerve fibers and of facilitating the processes of reinnervation, probably by means of an enhancement of fiber sprouting.

Alcoholism↗
PubMed1993

Gangliosides attenuate vincristine neurotoxicity on dorsal root ganglion cells.

We investigated the effects of bovine brain gangliosides on the neurotoxicity of vincristine in dissociated cultures of dorsal root ganglion cells from 10-day chick embryos. The effects of the drugs were quantified as the numbers of neurite-bearing cells or total neurite length in individual neurite-bearing cells. The administration of vincristine (1 to 1000 pg/mL) inhibited neurite outgrowth from the cells, whereas gangliosides (10 to 1000 micrograms/mL) protected them against this inhibition in a concentration-dependent manner. Electron microscopy revealed vincristine-induced fragmentation and longitudinal disorientation of microtubules in neurites and showed the protection by gangliosides against such damaging effects. Our results show that exogenous administration of gangliosides attenuates the neurotoxicity of vincristine in vitro.

Animals↗
PubMed1987

Effects of fimbria-fornix transection and ganglioside treatments on histochemical staining for glucose-6-phosphate dehydrogenase in the lateral septum.

The present study examined whether ganglioside treatments would affect an enzyme marker (glucose-6-phosphate dehydrogenase; G6PDH) of neural metabolism in an established model system (the hippocamposeptal projection) of deafferentation and sprouting. Rats were subjected to unilateral transections of the fimbria-fornix (FF) in order to (1) interrupt the hippocamposeptal projection, (2) deafferent the lateral septal nucleus (LSN) ipsilaterally, and (3) induce sprouting by the contralateral FF. In untreated rats which were killed at 2-4 days postlesion, histochemical staining for G6PDH was reduced by 35-40% in the deafferented LSN relative to the contralateral side. However, at 6-8 days (i.e., when sprouting begins), staining intensity returned toward contralateral values (i.e., recovered). This pattern of changes in G6PDH staining was not observed in the caudate nucleus adjacent to the LSN. In ganglioside-treated rats which were killed at 4 days, there was a significantly smaller reduction of G6PDH staining in the deafferented LSN (23%; P = .05). This effect was not observed in the LSN of treated rats killed at 2 days, nor in the caudate nucleus at either time point. The present data indicate that (1) FF transection results in a reduction and subsequent recovery of G6PDH staining in the deafferented LSN; and (2) ganglioside treatments may accelerate the onset of the recovery of G6PDH activity. We suggest that gangliosides' effect on G6PDH reflects an acute enhancement of biosynthetic events in deafferented neurons.

Afferent Pathways↗
PubMed2000

Ganglioside GD3 and its mimetics induce cytochrome c release from mitochondria.

Ganglioside GD3 induced the release of cytochrome c from isolated rat liver mitochondria. This process was completely prevented by cyclosporin A and partially prevented by a cysteine protease inhibitor, n-acetyl-leu-leu-norleucinal. Cyclosporin A is a potent inhibitor of the permeability transition pore, whereas n-acetyl-leu-leu-norleucinal has no effect on this pore. These results indicate that the release of cytochrome c from mitochondria requires both the opening of the permeability transition pore and a cysteine protease inhibitor-sensitive mechanism. Gangliosides GD1a, GD1b, GT1b, and GQ1b along with the synthetic GD3 mimetics TMS-42 and CI-22, which are glycerophospholipids carrying a disialo residue, also induced cytochrome c release. In contrast, gangliosides GM1, GM2, and GM3 did not induce cytochrome c release. These results indicate that two sialo residues must play an important role in the induction of cytochrome c release by gangliosides.

Animals↗
PubMed1976

Possible functional role of gangliosides.

The brain ganglioside pattern of taxonomically close and distant related fish living at different temperatures were compared with the mammalian pattern. Furthermore the goldfish brain pattern was investigated after adaption (acclimitization, acclimation) to different temperatures. The results demonstrate correlations between body temperature and brain gangliosides: the lower the body temperature of animals, the higher the relative proportion of multi-sialo-gangliosides. The results are discussed with respect to the possible functional role of Ca++-ganglioside-complexes for the process of synaptic transmission.

Acclimatization↗
PubMed1976

Interaction of cholera toxin and ganglioside G(M1).

The exotoxin produced by Vibrio cholerae is rapidly and firmly bound to the outer membrane of mammalian cells. With simple in vitro and in vivo methods and very pure gangliosides and allied glycolipids we have demonstrated that the monosialosylganglioside GM1 is the natural receptor for the cholera toxin. This ganglioside binds the toxin with a high affinity and inactivates it. The inactive derivative, choleragenoid toxoid has the same affinity to GM1 as the toxin. Ganglioside GM1 was isolated from the small intestinal mucosa of man, pig and ox in amounts of 0.1, 2.0 and 43 nmoles per g mucosa, respectively. These very large differences in the ability of the mucosal cells to bind cholera toxin. Exogenous GM1 was incorporated in vitro and in vivo in intestinal mucosal cells. The incorporation of GM1 increased the number of toxin-binding sites and increased the secretion of fluid in the gut. Vibrio cholerae sialidase did not hydrolyse the di- and trisialogangliosides of intact mucosal cells to the parent GM1-ganglioside, neither did it increase the number of cholera toxin-binding sites.

Animals↗
PubMed1991

Ganglioside antigens in tissue sections of skin, naevi, and melanoma--implications for treatment of melanoma.

The ganglioside GD3 was distributed widely on melanocytes, naevi, and practically all melanomas. Not all the cells in melanoma appeared to express GD3, so that treatment with MAbs to GD3 could be expected to leave foci of tumor cells resistant to the effects of the MAbs. GM3 had a similar distribution of GD3 on melanoma, but was expressed on a lower percentage of cells in individual tumors. Expression of GM3 appeared to be suppressed on melanoma and naevus cells in the epidermis. Addition of MAbs to GM3 to those against GD3 in the treatment of melanoma may increase the lytic effect against cells coexpressing both gangliosides, but as GM3 did not appear to be expressed on GM3 -ve cells, the percentage of resistant cells may not be decreased. GD2 was expressed on only approximately 25% of primaries and less than 50% of metastases. In individual tumors there was some evidence of reciprocal expression of GD3 and GD2, so the combination of MAbs to GD3 and GD2 may decrease the percentage of melanoma cells that are resistant to either MAb alone. Both GD3 and GD2, but not GM3, was expressed on lymphocytes around melanoma metastases in LNs and around melanomas in skin. GD2 was detected on a large percentage of lymphocytes around metastases in lymph nodes, but not in the skin, suggesting that the gangliosides GD2 and GD3 may be expressed on different subsets of T-lymphocytes. These findings, together with previous studies showing that the MAbs can enhance lymphocyte responses to a variety of stimuli, provide support for the hypothesis that the clinical effects of the MAbs may reflect activation of host responses against the tumor. Further analysis of the role of gangliosides in lymphocyte function is needed.

Antibodies, Monoclonal↗
PubMed1984

Cellular localization of gangliosides in the mouse cerebellum: analysis using neurological mutants.

We have used genetic dissection to study the cellular localization of gangliosides in the mouse cerebellum. This method employs a series of mouse mutations that destroy specific populations of cerebellar neurons at precise stages of development. By correlating the well documented histological changes occurring in these mutants with changes in ganglioside composition, we have obtained strong evidence for a non-random cellular distribution of gangliosides. Most notably, GD1a is more enriched in granule cells that in Purkinje cells, whereas the opposite is true for GT1a. GD3, on the other hand, is heavily enriched in reactive glia and may serve as a useful biochemical marker for the presence of reactive glia in neurological disease. The continued study of gangliosides in the various mouse mutants will help elucidate their cellular localization in the CNS.

Aging↗
PubMed1984

Immunological expression of gangliosides in multiple sclerosis and in a demyelinating model disease in rabbits.

Accumulating evidence suggests that the process of demyelination in MS might involve an autoimmune response to one or more myelin components. A combination of myelin basic protein and myelin haptens was considered as possibly enhancing a cellular or humoral autoimmune reaction in MS. In line with this motion we have used an in-vitro E-rosette assay that correlates with in-vivo delayed hypersensitivity to demonstrate specific immunologic sensitivity of lymphocytes from MS patients to polysialogangliosides. A recent report that only lymphocytes from patients in relapse, but not in remission, are primed by gangliosides, underscores the relevance of the antigenic expression of gangliosides during the active pathological phase of the disease. The antigenic capacity of gangliosides to induce upon immunization a neurological disorder featured by demyelination in the CNS was demonstrated in rabbits. This and previous reports on the induction of peripheral demyelination in rabbits immunized with gangliosides will be further analyzed to gain insight on the possible role of these myelin lipid components as targets for an autoimmune mechanism in MS.

Adult↗
PubMed1984

Studies of gangliosides in diverse nerve cell cultures.

Primary nerve cell cultures and tumor cells have been analysed with respect to synthesis of gangliosides. Neither developmental aspects of primary cultures nor nerve growth factor-induced fiber extension in PC12 or ZPH tumor cells gave any evidence of an involvement of gangliosides. Thus, it is concluded that neurite sprouting and ganglioside synthesis may not be interrelated, but that gangliosides might well serve as receptors for trophic factors.

Adrenal Gland Neoplasms↗
PubMed1984

Ganglioside treatment of genetic and alloxan-induced diabetic neuropathy.

Peripheral neuropathy is a common complication of diabetes. Using the mutant diabetic mouse C57BL/ks (db/db) and alloxan-treated rats, 30 days after intoxication, we investigated development and treatment with gangliosides of such a disease. The db/db mouse develops a neuropathy characterized by a loss in conduction velocity shown as early as 80-90 days after birth and maintained throughout life. At later stages (5-6 months of age) there is a drop in slow transport and myelin particle density. These changes are correlated by a lack of response to insulin treatment, which, prior to this stage, is capable of improving nerve conduction velocity (NCV). On the other hand gangliosides became effective, improving NCV, myelin particle density and sensory perception (auditory deficit) at 5 months of age in the db/db mouse. We presume that this differential neuronal response to insulin and gangliosides indicates a change of the neuropathy from a metabolic stage to neuronal. Alloxan induced diabetic neuropathy is treatable with gangliosides even 30 days after intoxication.

Acetylcholinesterase↗