Acute administration of cocaine reduces metabotropic glutamate receptor 8 protein expression in the rat striatum in vivo

Zhang, Guochi; Vu, Khang; Parelkar, Nikhil K.; Mao, Limin; Stanford, Ian M.; Fibuch, Eugene E.; Wang, John Q.

doi:10.1016/j.neulet.2008.11.008

Cited by 14 publications

(15 citation statements)

References 27 publications

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“…6 Quantification of the enzymatic activity to glutaminase in striatum (a) (n=6), hippocampus (b) (n=6) and prefrontal cortex (c) (n=6) after acute treatment vs. chronic pretreatment with vehicle and cocaine in mice. *p<0.05; ***p<0.001 restricted regional effects of cocaine has been found also in other members of the glutamate-signalling pathway such as the mGluR8 whose protein expression levels in the hippocampus and prefrontal cortex also remained constant after acute cocaine injection while they were downregulated in the striatum (Zhang et al 2009). …”

Section: Discussionmentioning

confidence: 93%

Cocaine modulates both glutaminase gene expression and glutaminase activity in the brain of cocaine-sensitized mice

Blanco

Campos-Sandoval

Palomino³

et al. 2011

Psychopharmacology

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Section: Discussionmentioning

confidence: 93%

Cocaine modulates both glutaminase gene expression and glutaminase activity in the brain of cocaine-sensitized mice

Blanco

Campos-Sandoval

Palomino³

et al. 2011

Psychopharmacology

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“…The molecular targets are often drug specific, for example, the dopamine transporter for cocaine and amphetamine exposure (Calipari, Ferris, Salahpour, Caron, & Jones, 2013; Peraile et al, 2010), opioid receptors and propeptide genes for opioid exposure (Diaz, Barros, Antonelli, Rubio, & Balerio, 2006), and GABA and glutamate receptors for other drug and alcohol exposure (Enoch et al, 2012; Meinhardt et al, 2013; Nona, Li, & Nobrega, 2013; Schumann & Yaka, 2009; Swanson, Baker, Carson, Worley, & Kalivas, 2001; Zhang et al, 2009; Zhou et al, 2013). Certain aspects of cell signaling, early transcriptional response, and learning have been obvious, and fruitful, targets for study in the addictions.…”

Section: Molecular Adaptations Accompanying Early Response and Lonmentioning

confidence: 99%

Gene Expression in the Addicted Brain

Zhou¹,

Enoch²,

Goldman³

2014

International Review of Neurobiology

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Addiction is due to changes in the structure and function of the brain, including neuronal networks and the cells that comprise them. Within cells, gene expression changes can track and help explain their altered function. Transcriptional changes induced by addictive agents are dynamic and divergent and range from signal pathway-specific perturbations to widespread molecular and cellular dysregulation that can be measured by “omic” methods and that can be used to identify new pathways. The molecular effects of addiction depend on timing of exposure or withdrawal, the stage of adaptation, the brain region, and the behavioral model, there being many models of addiction. However, the molecular neural adaptations across different drug exposures, conditions, and regions are to some extent shared and can reflect common actions on pathways relevant to addiction. Epigenetic studies of DNA methylation and histone modifications and studies of regulatory RNA networks have been informative for elucidating the mechanisms of transcriptional change in the addicted brain.

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“…drug addiction | histone methylation K nowledge of the cellular and molecular adaptations underlying addiction to cocaine and alcohol has primarily been gained from animal models of acute and chronic drug exposure, from which specific molecular pathways to addiction have been identified (1,2). Studies on human postmortem brain (3) have yielded data that are complementary and tend to validate animal models of exposure.…”

mentioning

confidence: 99%

Substance-specific and shared transcription and epigenetic changes in the human hippocampus chronically exposed to cocaine and alcohol

Zhou

Yuan

Mash

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

198

208

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The hippocampus is a key brain region involved in both short-and long-term memory processes and may play critical roles in drugassociated learning and addiction. Using whole genome sequencing of mRNA transcripts (RNA-Seq) and immunoprecipitation-enriched genomic DNA (ChIP-Seq) coupled with histone H3 lysine 4 trimethylation (H3K4me3), we found extensive hippocampal gene expression changes common to both cocaine-addicted and alcoholic individuals that may reflect neuronal adaptations common to both addictions. However, we also observed functional changes that were related only to long-term cocaine exposure, particularly the inhibition of mitochondrial inner membrane functions related to oxidative phosphorylation and energy metabolism, which has also been observed previously in neurodegenerative diseases. Cocaineand alcohol-related histone H3K4me3 changes highly overlapped, but greater effects were detected under cocaine exposure. There was no direct correlation, however, between either cocaine-or alcohol-related histone H3k4me3 and gene expression changes at an individual gene level, indicating that transcriptional regulation as well as drug-related gene expression changes are outcomes of a complex gene-regulatory process that includes multifaceted histone modifications.drug addiction | histone methylation K nowledge of the cellular and molecular adaptations underlying addiction to cocaine and alcohol has primarily been gained from animal models of acute and chronic drug exposure, from which specific molecular pathways to addiction have been identified (1, 2). Studies on human postmortem brain (3) have yielded data that are complementary and tend to validate animal models of exposure. Addiction-associated molecular alterations observed in animal and human studies are diverse. Clearly, cellular and molecular responses to addictive drugs depend on the type and timing of exposure, the timing of observations within the progression to addiction, and the brain regions and cells in which observations are made. Specific changes in signal transduction pathways, including in the transcription factor ΔFosB and the cAMP-response element binding protein (CREB), are likely to be more prominent in early stages of drug-induced neuroadaptation (4). Longstanding adaptations may be marked by changes in expression of genes involved in the regulation of cellular functions including ion transport, chromosome remodeling, stress and immune response, cell adhesion, cell cycle, apoptosis, protein and lipid metabolism, and mitochondrial functions (3). Later changes may be more closely relevant to addictive behaviors and long-lasting vulnerability to relapse.The hippocampus is also a brain region critically involved in addiction. Most studies have focused on the mesolimbic system, in which medium-sized spiny neurons in the dorsal striatum and nucleus accumbens mediate dopaminergic, glutamatergic, and GABAergic neurotransmission (5) and are key in drug-reward and drug-seeking behavior. However, hippocampal functions related to short-and long...

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Acute administration of cocaine reduces metabotropic glutamate receptor 8 protein expression in the rat striatum in vivo

Cited by 14 publications

References 27 publications

Cocaine modulates both glutaminase gene expression and glutaminase activity in the brain of cocaine-sensitized mice

Cocaine modulates both glutaminase gene expression and glutaminase activity in the brain of cocaine-sensitized mice

Gene Expression in the Addicted Brain

Substance-specific and shared transcription and epigenetic changes in the human hippocampus chronically exposed to cocaine and alcohol

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