GM1 ganglioside enhances the rewarding properties of cocaine in rats

Valdomero, Analía; Hansen, Cristian; Burgos, Nelia Gerez de; Cuadra, Gabriel; Orsingher, Otto A.

doi:10.1016/j.ejphar.2009.12.029

Cited by 9 publications

(11 citation statements)

References 18 publications

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“…In the present study, to confirm our hypothesis that exogenous GM1 may increase levels of BDNF protein in the NAc, we reproduced the same behavioral experimental conditions described previously [3] and then prepared the animals for the BDNF determination.…”

Section: Introductionsupporting

confidence: 59%

“…Its inhibitory effect on the dopamine transporter was also assessed. However, none of these parameters was modified by GM1 pretreatment [3]. Given that exogenous GM1 has neurotrophic properties, and that brain-derived neurotrophic factor (BDNF) plays an important role in various processes of cocaine addiction, we propose that the impact of GM1 on cocaine rewarding effects might be due to increased BDNF protein levels and/or the influence of BDNF action.…”

Section: Introductionmentioning

confidence: 96%

“…Taking into account that GM1 increases the rewarding properties of cocaine [3], that intra-NAc BDNF infusions increased the cocaine-induced response to the conditioned reinforcer [11], as well as the GM1-BDNF interaction mentioned above, it seems reasonable to propose that GM1 may alter BDNF expression in the reward circuitry. In the present study, to confirm our hypothesis that exogenous GM1 may increase levels of BDNF protein in the NAc, we reproduced the same behavioral experimental conditions described previously [3] and then prepared the animals for the BDNF determination.…”

Section: Introductionmentioning

confidence: 97%

See 2 more Smart Citations

Exogenous GM1 ganglioside increases accumbal BDNF levels in rats

Valdomero

Perondi

Orsingher

et al. 2015

Behavioural Brain Research

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Section: Introductionsupporting

confidence: 59%

Section: Introductionmentioning

confidence: 96%

Section: Introductionmentioning

confidence: 97%

See 1 more Smart Citation

Exogenous GM1 ganglioside increases accumbal BDNF levels in rats

Valdomero

Perondi

Orsingher

et al. 2015

Behavioural Brain Research

Self Cite

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“…been detected in the dentate gyrus of the hippocampus among patients with brain dysfunctions (7). It has been reported that mannose and polymannose penetrate the blood-brain barrier; on the other hand, it has been reported that GM1 ganglioside induces the cocaine transporter in the blood-brain barrier (10). These may suggest a mechanism for the subsidiary effect of the humoral Gal β1-3 GalNAc-lipid.…”

Section: Discussionmentioning

confidence: 92%

Humoral glycolipid is associated with mouse memory impairment caused by lipopolysaccharide

Masuda¹,

Sugiyama²

2013

Biomed. Res.

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Mouse memory impairment induced by repeated daily dosing of lipopolysaccharide from Escherichia coli 044 was investigated using a passive avoidance method. One dose of 25 mg/kg or 8 repeated daily doses of 2.5 mg/kg of the lipopolysaccharide impaired the memory of 6-week-old male ddY mice. The chemical structure of the lipopolysaccharide was polymannoses Gal β1-3 GalNAc-lipid A. Humoral polymannose-lipid reactivity was not found in lipopolysaccharide or in control mice receiving repeated daily doses of physiological saline. Humoral glycolipid with Gal β1-3 GalNAc reactivity was found in the mice repeatedly treated with the lipopolysaccharide but not in the control mice repeatedly treated with physiological saline. Intraperitoneal injection of the humoral glycolipid did not impair memory in the normal mice, but mice treated beforehand with the glycolipid showed memory impairment after a subsequent single injection of 2.5 mg/kg of the lipopolysaccharide. These findings suggest that the polymannose component of the lipopolysaccharide is closely associated with the memory impairment effect and that the humoral glycolipid is a subsidiary metabolite of the lipopolysaccharide.Studies have shown that high doses of lipopolysaccharides (LPS) induce mouse memory impairment (3, 11), and this has been compared to delirium caused by inflammation (2). However, some brain dysfunctions without brain lesions are thought to be associated with humoral glycolipids passing through the blood-brain barrier (4, 6); LPS are themselves glycolipids. These findings suggest that LPS impair memory by themselves and/or through metabolites, which are sugar chain structures. In the present study, we examined the effects of repeated treatment with LPS and detected the effective metabolite in mice. MATERIALS AND METHODDetection of mouse memory impairment. Mouse memory impairment was detected by the passive avoidance method using the Passive-through apparatus (Obara Ikasangyo, Osaka, Japan). The main component of the apparatus is a shuttle box consisting of a bright chamber and a dark chamber whose floor gives an electric shock (150 V, 1 mA, 50 Hz) to a mouse (Fig. 1). Mice originally prefer the dark chamber. Mice placed in the bright chamber enter the dark chamber within 30 s. Subsequently, they are given an electric shock in the dark chamber, after which they immediately return to the bright chamber. Mice memorize the electric shock and avoid entering the dark chamber in the next trial. When a mouse still enters the dark chamber within 30 s, it is considered to have impaired memory (5).

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“…For instance, repeated treatment with GM1 (30 mg/kg, IP for 7 days) attenuates amphetamine-induced locomotor sensitization in mice [31]. Moreover, pre-treatment with GM1 in rats enhances the rewarding property of cocaine as determined by conditioned place preference [32]. Although GM1 treatment does not alter the function and expression of DAT, it modifies the brain cocaine disposition by increasing brain cocaine levels.…”

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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GM1 ganglioside enhances the rewarding properties of cocaine in rats

Cited by 9 publications

References 18 publications

Exogenous GM1 ganglioside increases accumbal BDNF levels in rats

Exogenous GM1 ganglioside increases accumbal BDNF levels in rats

Humoral glycolipid is associated with mouse memory impairment caused by lipopolysaccharide

Psychostimulants, Brain Membrane Lipids and Dopamine Transmission

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