Enhancement of Depolarization‐Induced Release of γ‐Aminobutyric Acid from Brain Slices by Antibodies to Ganglioside

Frieder, Brina; Rapport, Maurice M.

doi:10.1111/j.1471-4159.1982.tb12534.x

Cited by 24 publications

(3 citation statements)

References 21 publications

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“…50 Such antibodies have been reported to increase release of neuronal GABA after depolarisation, possibly exerting a convulsant effect by interfering with kindling51 or inhibiting the interaction of GABA with synaptic receptors and/or transport sites 52. Anti-GM1 antibodies in peripheral neuropathies are thought to interfere with conduction by their action on voltage gated Na + and possibly K + channels of myelinated nerve fibres53; however, this mechanism of action has not been investigated in the CNS.…”

Section: Antibodies Associated With Unselected Patients With Epilepsymentioning

confidence: 99%

Epilepsy: an autoimmune disease?

Palace

2000

Journal of Neurology, Neurosurgery &Amp; Psychiatry

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Section: Antibodies Associated With Unselected Patients With Epilepsymentioning

confidence: 99%

Epilepsy: an autoimmune disease?

Palace

2000

Journal of Neurology, Neurosurgery &Amp; Psychiatry

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“…Subsequently GM1 ganglioside was found to be the receptor molecule for the cholera toxin [King and van Heyningen, 1973;Cuatrecasas, 1973;Staerk et al, 19741. It has been suggested that gangliosides play roles in synatpic transmission and memory generation, stimulate axonal outgrowth in culture, and promote axonal regeneration in vivo [Gorio et al, 1980;Frieder and Rapport, 1981;Morgan and Seifert, 1979;Roisen et al, 198 1 ;Ledeen et al, 19841. It is generally believed that most brain cell types contain similar patterns of ganglioside species [Hamberger and Svennerholm, 1971 ;Abe and Norton, 1974;Norton et al, 19751. There are, however, some disagreements concerning this view; the existence of differences in ganglioside distribution between various brain regions has been known [Suzuki, 1965;Seyfried et al, 1978;19821, as has the exclusive localization of GM4 ganglioside in myelin and oligodendrocytes isolated from human brains [Ledeen et al, 1973;Yu and Iqbal, 19791.…”

Section: Introductionmentioning

confidence: 98%

Neuroimmunology of gangliosides in human neurons and glial cells in culture

Kim

Moretto

Lee

et al. 1986

J of Neuroscience Research

100

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Gangliosides (sialic-acid-bearing glycolipids) have received attention in recent years because of their role in cell recognition phenomena, synaptic transmission, memory generation, and nerve regeneration in the fields of neurosciences. It is suggested that each brain region or each neural cell type may contain a specific and characteristic set of gangliosides. We have investigated the immunocytochemical localization of several classes of gangliosides that include GM1, GM4, GD3, and GQ gangliosides on the cell surface of various cell types found in human neural cell cultures with antibodies specific for these gangliosides. Cell cultures were obtained from adult human brains and fetal human dorsal root ganglia and spinal cord and cultured in vitro for the period up to 6 months and utilized for the ganglioside immunocytochemistry. It was demonstrated that GM1 ganglioside was present in all galactocerebroside-positive oligodendrocytes and most of glial fibrillary acid protein (GFAP)-positive astrocytes (80%), most of neurofilament-positive neurons (80%), 50-70% of Schwann cells, and 5-10% of fibronectin-positive fibroblasts; GM4 ganglioside could be detected in all oligodendrocytes, 80% of astrocytes, and 50% of Schwann cells, while no staining was found in neurons or fibroblasts; GD3 ganglioside was present in all oligodendrocytes and 5-10% of astrocytes but not in neurons, Schwann cells, or fibroblasts; and all of fetal CNS neurons and approximately 80-90% of fetal dorsal root ganglia (DRG) neurons and a small percentage of astrocytes (10-20% in fetal and less than 1% in adult astrocytes) was labeled by A2B5 antibody which is specific for GQ ganglioside, while this antibody did not stain cell surface of oligodendrocytes, Schwann cells, or fibroblasts. Three classes of gangliosides, GM1, GM4, and GD3 were found to be definite components of fetal and adult human oligodendroglial plasma membrane, while GM1 and GM4 gangliosides were detected on the surface of most astrocytes. Only a minor population of astrocytes from both fetal and adult human CNS contained GD3 and GQ gangliosides. Two classes of gangliosides, GM1 and GQ, were detected on the surface of fetal human neurons. More than half of fetal Schwann cells reacted to GM1 and GM4 antibodies but did not to GD3 or GQ antibodies. We recognized the presence of a specific and characteristic set of gangliosides on the cell surface of different human neural cell types and these findings should facilitate further investigation of the precise biological activity of these gangliosides.

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“…However, when monospecific antibodies to these antigens are obtained, they should be useful in providing additional evi-dence for synaptic localization by immunocytochemical techniques. Further, since antibodies to synaptic membrane constituents can affect synaptic functions such as uptake and release of neurotransmitters (Haglid et al, 1979;Hofstein et al, 1981;Frieder and Rapport, 1981) and behavioral performance (Rapport et al, 1978), the antibodies can be used t o relate antigenic structures to neurobiological processes, and thus attack the problem of functional assignment.…”

Section: Discussionmentioning

confidence: 99%

Synaptic Membrane Antigens in Developing Rat Brain Cerebral Cortex and Cerebellum

Mahadik

Korenovsky

Ciccarone

et al. 1982

Journal of Neurochemistry

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The contents of five synaptic membrane antigens (56K, 58K, 62K, 63K, and 64K) were determined in rat cerebral cortex and cerebellum at eight developmental time points: E9, E14, P < 1, P5, P14, P28, P60, and P180 (E, embryonic; P, postnatal). In cerebral cortex, the five antigens showed five different developmental patterns with respect both to specific content (i.e., quantity per unit of membrane) and total content (i.e., quantity per cortex). The 56K, 58K, and 62K polypeptides were first detected at E14, increased slightly to P5, then increased rapidly from P5 to P28 by 14‐, 11‐, and 18‐fold, respectively. From P28 to PI80, the patterns of these antigens showed very large differences. The 63K and 64K antigens were first detected at P14 and P28, respectively. The specific content of 63K antigen continued to increase steadily throughout adult life; in contrast, the specific content of the 64K antigen did not change appreciably. In cerebellum only three antigens (56K, 58K, and 62K) were detected. These three antigens showed different developmental patterns. The 56K polypeptide was first detected at E14; its specific content increased very rapidly to a maximum at P < 1; it then decreased, first slowly, and then more rapidly, disappearing at P60. The 58K polypeptide also was detectable at E14 and increased very rapidly to a maximum at P < 1. It then decreased markedly to P5, followed by an increase, returning almost to its maximum level at P14. It then slowly decreased disappearing at P180. The 62K antigen was first detected at P14 and then it slowly decreased with disappearance at P60. The patterns with respect to total contents per cerebellum were similar for the three antigens, with a maximum at P28. We conclude that the highest increase in the contents of these antigens roughly corresponds to the period of maximal synaptogenesis (P9 to P28) in both regions. Differences among developmental patterns probably reflect changing molecular machinery required for development and functional differentiation of synapses in different brain regions. The fine structure of these patterns suggests that the quantitative measurement of synaptic membrane antigens will be useful for delineating complex processes occurring during synaptogenesis.

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Enhancement of Depolarization‐Induced Release of γ‐Aminobutyric Acid from Brain Slices by Antibodies to Ganglioside

Cited by 24 publications

References 21 publications

Epilepsy: an autoimmune disease?

Epilepsy: an autoimmune disease?

Neuroimmunology of gangliosides in human neurons and glial cells in culture

Synaptic Membrane Antigens in Developing Rat Brain Cerebral Cortex and Cerebellum

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