Cocaine modifies brain lipidome in mice

Lin, Yiyun; Gu, Hui; Jiang, Linhong; Xu, Wei; Liu, Chunqi; Li, Yan; Qian, Xinying; Li, Dandan; Li, Zhuoling; Hu, Jing; Zhang, Huaqin; Guo, Wei; Zhao, Yinglan; Cen, Xiaobo

doi:10.1016/j.mcn.2017.08.004

Cited by 24 publications

(15 citation statements)

References 47 publications

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“…These similarities occurred despite differences between the behavioral regimens used as well as differences in the dose and frequency of cocaine administration (Bodzon‐Kulakowska et al, ). Another recent study showed the profound effect of cocaine on the brain lipidome in mice using behavioral models of CPP and locomotor sensitization (Lin et al, ). Lin et al () demonstrated significant decreases in ceramide and lysophospholipids accompanied by increases in PLs and polyunsaturated fatty acid (PUFA)‐containing PLs in the nucleus accumbens.…”

Section: Discussionmentioning

confidence: 99%

“…Following our initial report (Cummings et al, ), other investigators (Bodzon‐Kulakowska et al, ; Lin et al, ) have recently explored the effects of drug exposure on the brain lipidome. Here, in the present study, we assess brain region‐specific lipid remodeling within a rodent model of drug exposure.…”

Section: Introductionmentioning

confidence: 99%

“…Following our initial report (Cummings et al, 2015), other investigators (Bodzon-Kulakowska et al, 2017;Lin et al, 2017) have recently explored the effects of drug exposure on the brain lipidome.…”

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confidence: 99%

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Lipidomic changes in the rat hippocampus following cocaine conditioning, extinction, and reinstatement of drug‐seeking

et al. 2019

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IntroductionCocaine dependence affects millions of individuals worldwide; however, there are no pharmacotherapeutic and/or diagnostic solutions. Recent evidence suggests a role for lipid signaling in the development and maintenance of addiction, highlighting the need to understand how lipid remodeling mediates neuroadaptation after cocaine exposure.MethodsThis study utilized shotgun lipidomics to assess cocaine‐induced lipid remodeling in rats using a novel behavioral regimen that incorporated multiple sessions of extinction training and reinstatement testing.ResultsMass spectrometric imaging demonstrated widespread decreases in phospholipid (PL) abundance throughout the brain, and high‐spatial resolution matrix‐assisted laser desorption/ionization Fourier‐transform ion cyclotron resonance mass spectrometry indicated hippocampus‐specific PL alterations following cocaine exposure. We analyzed the expression of genes involved in hippocampal lipid metabolism and observed region‐specific regulation. In addition, we found that cocaine exposure differentially regulates mitochondrial biogenesis in the brain.ConclusionsThis work presents a comprehensive lipidomic assessment of cocaine‐induced lipid remodeling in the rat brain. Further, these findings indicate a potential interplay between CNS energetics and differential lipid regulation and suggest a role for cocaine in the maintenance of energy homeostasis.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Lipidomic changes in the rat hippocampus following cocaine conditioning, extinction, and reinstatement of drug‐seeking

et al. 2019

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“…Concerning addiction, while the study of the brain circuits relevant for addictive-like behaviors is fundamental for its understanding and devising new therapies, there are a number of studies that tackle the direct impact of addictive substances exposure on sphingolipid brain metabolism. For instance, chronic ethanol consumption was shown to upregulate ceramide levels and decrease sphingomyelin levels in adult mouse brain [ 195 ] and while binging ethanol consumption decreased ceramide levels, ethanol withdrawal increased ceramide levels in the mouse cortex [ 196 ]; methamphetamine-sensitized mice had higher degree changes in the hippocampus and PFC lipidome, showing in both, decreased LacCer levels [ 197 ]; cocaine conditioned mice have widespread lipidomic alterations in the nucleus accumbens, striatum, PFC and hippocampus, notably showing decreased ceramide levels [ 198 ]; and using mass spectrometry imaging, administration of morphine, cocaine, and amphetamine in rodents was shown to lead to increased brain sulfatide levels [ 198 ].…”

Section: Sphingolipids In Psychiatric Diseasesmentioning

confidence: 99%

Sphingolipids as prognostic biomarkers of neurodegeneration, neuroinflammation, and psychiatric diseases and their emerging role in lipidomic investigation methods

Kruining

Luo

Echten‐Deckert

et al. 2020

Advanced Drug Delivery Reviews

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Lipids play an important role in neurodegeneration, neuroinflammation, and psychiatric disorders and an imbalance in sphingolipid levels is associated with disease. Although early diagnosis and intervention of these disorders would clearly have favorable long-term outcomes, no diagnostic tests currently exist that can accurately identify people at risk. Reliable prognostic biomarkers that are easily accessible would be beneficial to determine therapy and treatment response in clinical trials. Recent advances in lipidomic investigation methods have greatly progressed the knowledge of sphingolipids in neurodegenerative and psychiatric disorders over the past decades although more longitudinal studies are needed to understand its exact role in these disorders to be used as potential tools in the clinic. In this review, we give an overview of the current knowledge of sphingolipids in neurodegenerative and psychiatric disorders and explore recent advances in investigation methods. Finally, the potential of sphingolipid metabolism products and signaling molecules as potential biomarkers for diagnosis, prognostic, or surrogate markers of treatment response is discussed.

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“…Cx43 can affect the protein expression of EAATs but EAAT2 does not affect the expression of Cx43 protein. Spinal dorsal horn Cx43-EAATs may play a role in cancerous outbreaks [24].…”

Section: Mechanisms Of Breakthrough Cancer Painmentioning

confidence: 99%

Breakthrough Cancer Pain

Yan¹

2019

From Conventional to Innovative Approaches for Pain Treatment

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Breakthrough cancer pain has attracted more and more attentions recently because it has become the biggest obstacle to control cancer pain. Pain can occur at any stage of cancer. Despite the aggressive treatment, some patients still experience high-intensity pain in the short term, which is commonly referred to as breakthrough pain. Typical breakthrough pain has clinical features such as rapid onset and short duration, and it has uncontrollable and unpredictable characteristics, which impact the overall life quality of patients and the therapeutic effect of cancer pain. It has always been a puzzle and difficult in clinical treatment of breakthrough cancer pain. This paper aims to provide a more detailed review of the definition, assessment tools, classification and characteristics, epidemiology, and mechanism and treatment of breakthrough cancer pain, in order to facilitate the future development of this work in clinical treatment.

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Cocaine modifies brain lipidome in mice

Cited by 24 publications

References 47 publications

Lipidomic changes in the rat hippocampus following cocaine conditioning, extinction, and reinstatement of drug‐seeking

Lipidomic changes in the rat hippocampus following cocaine conditioning, extinction, and reinstatement of drug‐seeking

Sphingolipids as prognostic biomarkers of neurodegeneration, neuroinflammation, and psychiatric diseases and their emerging role in lipidomic investigation methods

Breakthrough Cancer Pain

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