Low-level developmental lead exposure does not predispose to adult alcohol self-administration, but does increase the risk of relapsing to alcohol seeking in mice: Contrasting role of GLT1 and xCT brain expression

Rangel‐Barajas, Claudia; Coronel, Israel; Zhang, Yanping; Hernández, Maribel; Boehm, Stephen L.

doi:10.1016/j.neuropharm.2020.108339

Cited by 6 publications

(3 citation statements)

References 70 publications

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“…Indeed, increased levels of xCT are observed in ethanol‐dependent rats, and the opposite is observed once rats are placed into withdrawal 39 . xCT upregulation in the NAc is also associated with an increased risk for relapse to alcohol seeking in mice 41 . Thus, it would appear that upregulation of accumbal xCT levels promotes vulnerability to addiction‐like behaviour.…”

Section: Discussionmentioning

confidence: 99%

“…39 xCT upregulation in the NAc is also associated with an increased risk for relapse to alcohol seeking in mice. 41 Thus, it would appear that upregulation of accumbal xCT levels promotes vulnerability to addiction-like behaviour. In contrast to xCT, no changes were observed in NAc expression of GLT1.…”

Section: Dio Rats Display Xct Upregulation In the Nucleus Accumbens B...mentioning

confidence: 99%

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Compulsive‐like eating of high‐fat high‐sugar food is associated with ‘addiction‐like’ glutamatergic dysfunction in obesity prone rats

et al. 2022

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Chronic overeating is a core feature of diet‐induced obesity. There is increasing evidence that in vulnerable individuals, such overeating could become compulsive, resembling an addictive disorder. The transition to compulsive substance use has been linked with changes at glutamatergic synapses in the nucleus accumbens. In this study, we investigated a potential link between such glutamatergic dysregulation and compulsive‐like eating using a rat model of diet‐induced obesity. A conditioned suppression task demonstrated that diet‐induced obese rats display eating despite negative consequences, as their consumption was insensitive to an aversive cue. Moreover, nucleus accumbens expression of GluA1 and xCT proteins was upregulated in diet‐induced obese animals. Lastly, both a computed ‘addiction score’ (based on performance across three criteria) and weight gain were positively correlated with changes in GluA1 and xCT expression in the nucleus accumbens. These data demonstrate that the propensity for diet‐induced obesity is associated with compulsive‐like eating of highly palatable food and is accompanied by ‘addiction‐like’ glutamatergic dysregulation in the nucleus accumbens, thus providing neurobiological evidence of addiction‐like pathology in this model of obesity.

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Section: Discussionmentioning

confidence: 99%

Section: Dio Rats Display Xct Upregulation In the Nucleus Accumbens B...mentioning

confidence: 99%

Compulsive‐like eating of high‐fat high‐sugar food is associated with ‘addiction‐like’ glutamatergic dysfunction in obesity prone rats

et al. 2022

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“…Several studies have been performed, examining the co-exposure of lead and alcohol, but the influence of arsenic has been less elucidated. Considering the prevalence of excessive alcohol and arsenic toxicity [19][20][21][22][23], the potential co-exposure, and the impact of both on hippocampal integrity, this study seeks to determine whether alcohol and arsenic combine to exacerbate neurodegeneration, microglial activation, and oxidative stress.…”

Section: Introductionmentioning

confidence: 99%

The Influence of Arsenic Co-Exposure in a Model of Alcohol-Induced Neurodegeneration in C57BL/6J Mice

Sides,

Nelson,

Nwachukwu

et al. 2023

Brain Sciences

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Both excessive alcohol consumption and exposure to high levels of arsenic can lead to neurodegeneration, especially in the hippocampus. Co-exposure to arsenic and alcohol can occur because an individual with an Alcohol Use Disorder (AUD) is exposed to arsenic in their drinking water or food or because of arsenic found directly in alcoholic beverages. This study aims to determine if co-exposure to alcohol and arsenic leads to worse outcomes in neurodegeneration and associated mechanisms that could lead to cell death. To study this, mice were exposed to a 10-day gavage model of alcohol-induced neurodegeneration with varying doses of arsenic (0, 0.005, 2.5, or 10 mg/kg). The following were examined after the last dose of ethanol: (1) microglia activation assessed via immunohistochemical detection of Iba-1, (2) reactive oxygen and nitrogen species (ROS/RNS) using a colorimetric assay, (3) neurodegeneration using Fluoro-Jade® C staining (FJC), and 4) arsenic absorption using ICP-MS. After exposure, there was an additive effect of the highest dose of arsenic (10 mg/kg) in the dentate gyrus of alcohol-induced FJC+ cells. This additional cell loss may have been due to the observed increase in microglial reactivity or increased arsenic absorption following co-exposure to ethanol and arsenic. The data also showed that arsenic caused an increase in CYP2E1 expression and ROS/RNS production in the hippocampus which could have independently contributed to increased neurodegeneration. Altogether, these findings suggest a potential cyclical impact of co-exposure to arsenic and ethanol as ethanol increases arsenic absorption but arsenic also enhances alcohol’s deleterious effects in the CNS.

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Forecasting and analysis of the effect of lifestyle on cognitive dysfunction induced by occupational aluminum exposure based on Bayesian networks

Zhao

Han

Huan

et al. 2023

Environmental Toxicology and Pharmacology

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Low-level developmental lead exposure does not predispose to adult alcohol self-administration, but does increase the risk of relapsing to alcohol seeking in mice: Contrasting role of GLT1 and xCT brain expression

Cited by 6 publications

References 70 publications

Compulsive‐like eating of high‐fat high‐sugar food is associated with ‘addiction‐like’ glutamatergic dysfunction in obesity prone rats

Compulsive‐like eating of high‐fat high‐sugar food is associated with ‘addiction‐like’ glutamatergic dysfunction in obesity prone rats

The Influence of Arsenic Co-Exposure in a Model of Alcohol-Induced Neurodegeneration in C57BL/6J Mice

Forecasting and analysis of the effect of lifestyle on cognitive dysfunction induced by occupational aluminum exposure based on Bayesian networks

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