Gangliosides and synaptic transmission

Thomas, Panakkezhum D.; Brewer, Gregory J.

doi:10.1016/0304-4157(90)90013-3

Cited by 60 publications

(24 citation statements)

References 193 publications

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“…Several studies have confirmed this strong binding and also that the apparent association constant depends on the surrounding ionic strength [22]. Svennerholm [23] suggested that Ca 2+ -associated gangliosides on the outer surface of the presynaptic membranes might be replaced by Na + as counter-ion by the action potential; this would facilitate transformation of the membrane lipid bilayer into a micellar state necessary for the fusion of the synaptic vesicle and the plasma membrane and release of transmitter.…”

Section: Discussionmentioning

confidence: 97%

Alzheimer Disease – Effect of Continuous Intracerebroventricular Treatment with GM1 Ganglioside and a Systematic Activation Programme

Svennerholm¹,

Bråne²,

Karlsson³

et al. 2002

Dement Geriatr Cogn Disord

116

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Five patients with the early-onset form of Alzheimer disease (AD) received GM1 ganglioside by continuous injection into the frontal horns of the lateral ventricles for a period of 12 months. The optimal GM1 dose varied between 20 and 30 mg/24 h. The patients were trained twice a week for 4–5 h with an individually designed cognitive programme, which included the use of a word processor. Neurological, neuropsychological, psychiatric and neurochemical examinations were performed a week before surgery and on days 30, 90, 180, 270 and 365 after surgery. The cerebrospinal fluid levels of the monoamine metabolites homovanillic acid and 5-hydroxyindoleacetic acid and the neuropeptide somatostatin increased. The regional cerebral blood flow showed a tendency to increase. The progression of deterioration was stopped, and motor performance and neuropsychological assessments improved. The patients became more active and felt safer in relation to other people and performing various activities. They had improved reading comprehension and a better feeling for language. They were able to write reports and short letters on a word processor. When interviewed at the end of the study, all 5 patients stated that they felt better, and their relatives reported that they had regained integrity and their joie de vivre.

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Section: Discussionmentioning

confidence: 97%

Alzheimer Disease – Effect of Continuous Intracerebroventricular Treatment with GM1 Ganglioside and a Systematic Activation Programme

Svennerholm¹,

Bråne²,

Karlsson³

et al. 2002

Dement Geriatr Cogn Disord

116

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“…In the human brain, GM3 is a minor ganglioside, which, in marked contrast with the major ganglioside species GM1 and GD1a, shows a regular increase with age. 35 Gangliosides are critical for neuronal integrity and plasticity 36 and synaptic function, 37 and have been involved in several neurodegenerative disorders, including Alzheimer's disease. 38,39 Circular dichroism experiments showed that GM1 can interact with α-syn and inhibit its fibrillation.…”

Section: Discussionmentioning

confidence: 99%

Altered Ion Channel Formation by the Parkinson's-Disease-Linked E46K Mutant of α-Synuclein Is Corrected by GM3 but Not by GM1 Gangliosides

Pasquale

Fantini

Chahinian

et al. 2010

Journal of Molecular Biology

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“…Since (1) the inhibitory activity of TN-C is neutralized by disialogangliosides and (2) disialogangliosides do not affect cell attachment to heparin binding fragments of FN (Stallcup, 1988; the present study), inhibition of neurite outgrowth is most likely due to an interference with the RGD-dependent, integrin-mediated process. The role of cell surface gangliosides in inducing neurite outgrowth and supporting reinnervation has been demonstrated in a number of studies (reviewed by Hakomori, 1990;Thomas and Brewer, 1990). In this respect, (1) the neurite outgrowth promoting activity of TN-C and TNfnD-containing protein fragments (Wehrle-Haller and Chiquet, 1993;Götz et al, 1996;Fischer et al, 1997) and (2) the involvement of the protein epitope recognized by antibody J1/tn2 in this process (Lochter et al, 1991;Götz et al, 1996Götz et al, , 1997 and ganglioside-mediated interactions of cells with TN-C (the present study) suggest a ganglioside-dependent mechanism of TN-C action in neuritogenesis.…”

Section: Discussionmentioning

confidence: 99%

Tenascin-C inhibits 1 integrin-dependent cell adhesion and neurite outgrowth on fibronectin by a disialoganglioside-mediated signaling mechanism

Probstmeier

Pesheva²

1999

Glycobiology

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We have previously shown that the extracellular matrix molecule tenascin-C inhibits fibronectin-mediated cell adhesion and neurite outgrowth by an interaction with a cellular RGDindependent receptor which interferes with the adhesion and neurite outgrowth promoting activities of the fibronectin receptor(s). Here we demonstrate that the inhibitory effect of tenascin-C on β 1 integrin-dependent cell adhesion and neurite outgrowth is mediated by the interaction of the protein with membrane-associated disialogangliosides, which interferes with protein kinase C-related signaling pathways. First, in substratum mixtures with fibronectin, an RGD sequencecontaining fragment of the molecule or synthetic peptide, tenascin-C inhibited cell adhesion and spreading by a disialoganglioside-dependent, sialidase-sensitive mechanism leading to an inhibition of protein kinase C. Second, the interaction of intact or trypsinized, i.e., cell surface glycoproteinfree, cells with immobilized tenascin-C was strongly inhibited by gangliosides or antibodies to gangliosides and tenascin-C. Third, preincubation of immobilized tenascin-C with soluble disialogangliosides resulted in a delayed cell detachment as a function of time. Similar to tenascin-C, immobilized antibody to GD2 (3F8) or sphingosine, a protein kinase C inhibitor, strongly inhibited RGD-dependent cell spreading. Finally, the degree of tenascin-C-induced inhibition of cell adhesion was proportional to the degree of disialoganglioside levels of expression by different cells suggesting the relevance of such mechanism in modulating integrin-mediated cell-matrix interactions during pattern formation or tumor progression.

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Gangliosides and synaptic transmission

Cited by 60 publications

References 193 publications

Alzheimer Disease – Effect of Continuous Intracerebroventricular Treatment with GM1 Ganglioside and a Systematic Activation Programme

Alzheimer Disease – Effect of Continuous Intracerebroventricular Treatment with GM1 Ganglioside and a Systematic Activation Programme

Altered Ion Channel Formation by the Parkinson's-Disease-Linked E46K Mutant of α-Synuclein Is Corrected by GM3 but Not by GM1 Gangliosides

Tenascin-C inhibits 1 integrin-dependent cell adhesion and neurite outgrowth on fibronectin by a disialoganglioside-mediated signaling mechanism

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