1H NMR-based metabonomics in brain nucleus accumbens and striatum following repeated cocaine treatment in rats

Li, Y.; Yan, Gen; Zhou, Jixiang; Bu, Qian; Deng, Pengchi; Yang, Yanzhu; Deng, Yi; Zhao, Jinxuan; Shao, Xue; Zhu, Rui; Huang, Yina; Zhao, Yinglan; Cen, Xiaobo

doi:10.1016/j.neuroscience.2012.05.019

Cited by 29 publications

(22 citation statements)

References 61 publications

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“…CSAD is the rate-limiting enzyme in the biosynthesis of taurine, an antioxidant and agonist of glycine receptors (Wang et al, 2005). Acute cocaine exposure has been shown to decrease taurine tissue concentration in the rat NAcc at 2 h post injection (Li et al, 2012). Additionally, repeated cocaine was shown to increase extracellular release of taurine at 30 min post injection (Yablonsky-Alter et al, 2009).…”

Section: Discussionmentioning

confidence: 99%

Environmental enrichment alters protein expression as well as the proteomic response to cocaine in rat nucleus accumbens

Lichti

Fan

English

et al. 2014

Front. Behav. Neurosci.

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Prior research demonstrated that environmental enrichment creates individual differences in behavior leading to a protective addiction phenotype in rats. Understanding the mechanisms underlying this phenotype will guide selection of targets for much-needed novel pharmacotherapeutics. The current study investigates differences in proteome expression in the nucleus accumbens of enriched and isolated rats and the proteomic response to cocaine self-administration using a liquid chromatography mass spectrometry (LCMS) technique to quantify 1917 proteins. Results of complementary Ingenuity Pathways Analyses (IPA) and gene set enrichment analyses (GSEA), both performed using protein quantitative data, demonstrate that cocaine increases vesicular transporters for dopamine and glutamate as well as increasing proteins in the RhoA pathway. Further, cocaine regulates proteins related to ERK, CREB and AKT signaling. Environmental enrichment altered expression of a large number of proteins implicated in a diverse number of neuronal functions (e.g., energy production, mRNA splicing, and ubiquitination), molecular cascades (e.g., protein kinases), psychiatric disorders (e.g., mood disorders), and neurodegenerative diseases (e.g., Huntington's and Alzheimer's diseases). Upregulation of energy metabolism components in EC rats was verified using RNA sequencing. Most of the biological functions and pathways listed above were also identified in the Cocaine X Enrichment interaction analysis, providing clear evidence that enriched and isolated rats respond quite differently to cocaine exposure. The overall impression of the current results is that enriched saline-administering rats have a unique proteomic complement compared to enriched cocaine-administering rats as well as saline and cocaine-taking isolated rats. These results identify possible mechanisms of the protective phenotype and provide fertile soil for developing novel pharmacotherapeutics. Proteomics data are available via ProteomeXchange with identifier PXD000990.

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Section: Discussionmentioning

confidence: 99%

Environmental enrichment alters protein expression as well as the proteomic response to cocaine in rat nucleus accumbens

Lichti

Fan

English

et al. 2014

Front. Behav. Neurosci.

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“…Yet the role of cocaine on facilitating reward or relapse behaviors with respect to mitochondrial oxidative stress is not clear. So far, it appears that mitochondrial oxidative stress and associated apoptosis can occur in animals who exhibited preference for cocaine in the conditioned place preference (CPP) test (Li et al, 2012). Further, a recent study shows increased copy numbers of mtDNA and gene expression in animals that went through an extinction training in an operant cocaine self-administration paradigm (Sadakierska-Chudy et al, 2016) (Fig.…”

Section: Sudmentioning

confidence: 99%

Sex-dependent mental illnesses and mitochondria

Shimamoto

Rappeneau

2017

Schizophrenia Research

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The prevalence of some mental illnesses, including major depression, anxiety-, trauma-, and stress-related disorders, some substance use disorders, and later onset of schizophrenia, is higher in women than men. While the higher prevalence in women could simply be explained by socioeconomic determinants, such as income, social status, or cultural background, extensive studies show sex differences in biological, pharmacokinetic, and pharmacological factors contribute to females’ vulnerability to these mental illnesses. In this review, we focus on estrogens, chronic stress, and neurotoxicity from behavioral, pharmacological, biological, and molecular perspectives to delineate the sex differences in these mental illnesses. Particularly, we investigate a possible role of mitochondrial function, including biosynthesis, bioenergetics, and signaling, on mediating the sex differences in psychiatric disorders.

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“…Additionally, Nuclear magnetic resonance (NMR) spectroscopy technique, one of the most commonly used analytical methods in metabonomic study, has been extensively used to investigate the variation of whole metabolites in brain tissues [15]. By using 1 H NMR-based on metabonomics, some researches showed that neurotransmitter pathways and energy metabolism are affected by addictive substances, such as morphine and cocaine [16], [17].…”

Section: Introductionmentioning

confidence: 99%

Mechanisms of Metabonomic for a Gateway Drug: Nicotine Priming Enhances Behavioral Response to Cocaine with Modification in Energy Metabolism and Neurotransmitter Level

Bu²,

Chen³

et al. 2014

PLoS ONE

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Nicotine, one of the most commonly used drugs, has become a major concern because tobacco serves as a gateway drug and is linked to illicit drug abuse, such as cocaine and marijuana. However, previous studies mainly focused on certain genes or neurotransmitters which have already been known to participate in drug addiction, lacking endogenous metabolic profiling in a global view. To further explore the mechanism by which nicotine modifies the response to cocaine, we developed two conditioned place preference (CPP) models in mice. In threshold dose model, mice were pretreated with nicotine, followed by cocaine treatment at the dose of 2 mg/kg, a threshold dose of cocaine to induce CPP in mice. In high-dose model, mice were only treated with 20 mg/kg cocaine, which induced a significant CPP. 1H nuclear magnetic resonance based on metabonomics was used to investigate metabolic profiles of the nucleus accumbens (NAc) and striatum. We found that nicotine pretreatment dramatically increased CPP induced by 2 mg/kg cocaine, which was similar to 20 mg/kg cocaine-induced CPP. Interestingly, metabolic profiles showed considerable overlap between these two models. These overlapped metabolites mainly included neurotransmitters as well as the molecules participating in energy homeostasis and cellular metabolism. Our results show that the reinforcing effect of nicotine on behavioral response to cocaine may attribute to the modification of some specific metabolites in NAc and striatum, thus creating a favorable metabolic environment for enhancing conditioned rewarding effect of cocaine. Our findings provide an insight into the effect of cigarette smoking on cocaine dependence and the underlying mechanism.

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1H NMR-based metabonomics in brain nucleus accumbens and striatum following repeated cocaine treatment in rats

Cited by 29 publications

References 61 publications

Environmental enrichment alters protein expression as well as the proteomic response to cocaine in rat nucleus accumbens

Environmental enrichment alters protein expression as well as the proteomic response to cocaine in rat nucleus accumbens

Sex-dependent mental illnesses and mitochondria

Mechanisms of Metabonomic for a Gateway Drug: Nicotine Priming Enhances Behavioral Response to Cocaine with Modification in Energy Metabolism and Neurotransmitter Level

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