Cocaine exposure during pregnancy affects rat neonate and maternal brain glycosphingolipids

Leskawa, Kenneth C.; Jackson, Gabrielle; Moody, Carole A.; Spear, Linda P.

doi:10.1016/0361-9230(94)90251-8

Cited by 9 publications

(3 citation statements)

References 42 publications

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“…Moreover, cocaine rapidly concentrates into cells (Nassogne et al, 2004) and activates sigma-1 receptors which, in turn, increases plasma membrane LRs (Hayashi and Su, 2005). These data are also confirmed by "in vivo" studies showing that exposure to cocaine can induce marked changes in ganglioside composition in different areas of the brain (Leskawa et al, 1994). Cocaine influence on LR expression could account, at least in part, for the increased TNT formation that we observed at the lowest concentration used (150 nM).…”

Section: Discussionsupporting

confidence: 83%

In Vitro Effects of Cocaine on Tunneling Nanotube Formation and Extracellular Vesicle Release in Glioblastoma Cell Cultures

et al. 2014

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The effects of cocaine (150 nM, 300 nM, and 150 μM) on human glioblastoma cell cultures were studied on tunneling nanotube formation (1-h cocaine treatment) and extracellular vesicle release (1-, 3-, and 8-h cocaine treatment). Cocaine significantly increased the number of tunneling nanotubes only at the lowest concentration used. The release of extracellular vesicles (mainly exosomes) into the medium was stimulated by cocaine at each concentration used with a maximum effect at the highest concentration tested (150 μM). Moreover, cocaine (150 nM) significantly increased the number of vesicles with 61-80 nm diameter while at concentrations of 300 nM and 150 μM, and the smaller vesicles (30-40 nm diameter) were significantly increased with a reduction of the larger vesicles (41-60 nm diameter). A time dependence in the release of extracellular vesicles was observed. In view of the proposed role of these novel intercellular communication modes in the glial-neuronal plasticity, it seems possible that they can participate in the processes leading to cocaine addiction. The molecular target/s involved in these cocaine effects could be specific molecular components of plasma membrane lipid rafts and/or cocaine-induced modifications in cytoplasmic lipid composition.

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Section: Discussionsupporting

confidence: 83%

In Vitro Effects of Cocaine on Tunneling Nanotube Formation and Extracellular Vesicle Release in Glioblastoma Cell Cultures

et al. 2014

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“…However, by postnatal day 11, these two compounds return to control levels. 58 Neuronal migration and differentiation in the developing central nervous system involve delicately timed sequences of molecular signals. Membrane glycoconjugates are known to act as recognition signals in many cellular systems.…”

Section: Experimental Evidence Of Neuroteratogenic Effects Of Cocainementioning

confidence: 99%

Selective Direct Toxicity of Cocaine on Fetal Mouse Neurons: Teratogenic Implications of Neurite and Apoptotic Neuronal Loss

Nassogne

Evrard²,

Courtoy

1998

Annals of the New York Academy of Sciences

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This chapter reviews epidemiologic clinical surveys and experimental animal studies, indicating that cocaine may induce severe teratogenic effects on the developing brain. Evidence for direct toxic effects is next presented. Using cocultures of embryonic brain cells, we demonstrate that cocaine selectively affects neuronal cells, first causing a dramatic reduction in the number and length of neurites, then extensive neuronal death by apoptosis. By contrast, cocaine affected neither the abundance of astroglial cells nor their glial fibrillary acidic protein content. These effects are not due to cocaine metabolites. The contributions of indirect and direct effects that could account for cocaine neuroteratogenicity are finally discussed.

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“…Additionally, limited data have shown alterations in brain gangliosides, a group of glycosphingolipids. For example, rat offspring exposed to cocaine in utero show elevated levels of total gangliosides and glycosphingolipids [29]. Moreover, chronic amphetamine treatment (IP, 20 days) modulates the ganglioside profile of rat frontal cortex, in which the level of quadrisialoganglioside is increased whereas GD1, GM2 and GM3 are decreased [30].…”

Section: Cholesterol Content and The Function Of Transporters/ Receptorsmentioning

confidence: 99%

Psychostimulants, Brain Membrane Lipids and Dopamine Transmission

Chen¹

2016

J Biomol Res Ther

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Membrane lipids in the brain play important roles in regulation of the membrane compartmentalization, function and signaling of neurotransmitter transporters and receptors. This review summarizes findings on changes in the composition and metabolism of brain membrane lipids such as phospholipids, cholesterol and sphingolipids following chronic exposure to psychostimulants. We also discussed the mechanisms by which membrane lipids regulate the membrane compartmentalization and function of dopamine transports and receptors in animal brain tissues and cultured cell lines. This review indicates that chronic psychostimulant exposure causes the remodeling of brain membrane lipid, which may contribute to psychostimulant-induced functional alterations in dopamine transporters and receptors. Brain membrane lipids could be exploited as a new avenue for pharmacological interventions of abnormal brain dopamine transmission and dopamine-related addiction behavior.

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Cocaine exposure during pregnancy affects rat neonate and maternal brain glycosphingolipids

Cited by 9 publications

References 42 publications

In Vitro Effects of Cocaine on Tunneling Nanotube Formation and Extracellular Vesicle Release in Glioblastoma Cell Cultures

In Vitro Effects of Cocaine on Tunneling Nanotube Formation and Extracellular Vesicle Release in Glioblastoma Cell Cultures

Selective Direct Toxicity of Cocaine on Fetal Mouse Neurons: Teratogenic Implications of Neurite and Apoptotic Neuronal Loss

Psychostimulants, Brain Membrane Lipids and Dopamine Transmission

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