Activation of c-Jun N-terminal kinase is required for the regulation of endoplasmic reticulum stress response in the rat dorsal striatum following repeated cocaine administration

Go, Bok Soon; Ahn, Sung Min; Shim, Insop; Choe, Eun Sang

doi:10.1016/j.neuropharm.2010.04.009

Cited by 16 publications

(19 citation statements)

References 20 publications

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“…Overexpression of IRE1, an ER stress-related protein, induces JNK phosphorylation, leading to the upregulation of the ER stress response protein expression in non-neuronal cells [23]. Inhibition of JNK downregulates BiP overexpression after repeated cocaine exposure in the dorsal striatum [8]. Consistent with these data, the present study demonstrated that inhibition of JNK prior to cocaine challenge downregulates the cocaine challenge-induced increase in BiP expression in the NAc.…”

Section: Discussionsupporting

confidence: 87%

“…For instance, overstimulation of inotropic glutamate receptors leads to the disturbance of intracellular Ca 2+ in the ER, contributing to neuronal cell death [7,20]. Either acute or repeated cocaine administration upregulates the expression of the ER stress response proteins, BiP and caspase-12, via stimulation of NMDA receptors in the dorsal striatum [2,8,22]. In this study, blockade of NMDA receptors decreased the cocaine challenge-induced increase in BiP expression.…”

Section: Discussionmentioning

confidence: 52%

“…Since changes in cytosolic Ca 2+ concentrations and JNK phosphorylation after repeated cocaine upregulate BiP expression in the dorsal striatum [8], the involvement of JNK phosphorylation in the regulation of the ER stress response after a renewed Fig. 3.…”

Section: Resultsmentioning

confidence: 99%

“…Cocaine (Balgopia, Louvain-La-Neuve, Belgium) was dissolved in physiological saline (0.9% NaCl). The doses or concentrations of the reagents were determined from previous studies [2,5,8]. Rats were received repeated intraperitoneal (i.p.)…”

Section: Methodsmentioning

confidence: 99%

“…Previous studies have demonstrated that repeated cocaine administration upregulates the expression of mRNAs and proteins for the ER stress response in the NAc and the dorsal striatum, respectively [2,3,18,22] c-Jun N-terminal kinase (JNK) linked to dopamine D1 receptors and glutamate receptors leads to the ER stress response after repeated cocaine administration in a Ca 2+ -dependent manner [8]. Cocaine withdrawal has shown remarkable decreases in the functions of Ca 2+ channels in the NAc [9].…”

Section: Introductionmentioning

confidence: 99%

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Cocaine challenge increases the expression of immunoglobulin heavy chain binding protein in the rat nucleus accumbens

Ryu

Choe

2014

Neuroscience Letters

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Section: Discussionsupporting

confidence: 87%

Section: Discussionmentioning

confidence: 52%

Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Cocaine challenge increases the expression of immunoglobulin heavy chain binding protein in the rat nucleus accumbens

Ryu

Choe

2014

Neuroscience Letters

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Role of Endoplasmic Reticulum (ER) Stress in Cocaine-Induced Microglial Cell Death

Costa

Yao

Lü

et al. 2013

J Neuroimmune Pharmacol

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While it has been well-documented that drugs of abuse such as cocaine can enhance progression of human immunodeficiency virus (HIV)-associated neuropathological disorders, the underlying mechanisms mediating these effects remain poorly understood. The present study was undertaken to examine the effects of cocaine on microglial viability. Herein we demonstrate that exposure of microglial cell line-BV2 or rat primary microglia to exogenous cocaine resulted in decreased cell viability as determined by MTS and TUNEL assays. Microglial toxicity of cocaine was accompanied by an increase in the expression of cleaved caspase-3 as demonstrated by western blot assays. Furthermore, increased microglial toxicity was also associated with a concomitant increase in the production of intracellular reactive oxygen species, an effect that was ameliorated in cells pretreated with NADPH oxidase inhibitor apocynin, thus emphasizing the role of oxidative stress in this process. A novel finding of this study was the involvement of endoplasmic reticulum (ER) signaling mediators such as PERK, Elf2α, and CHOP, which were up regulated in cells exposed to cocaine. Reciprocally, blocking CHOP expression using siRNA ameliorated cocaine-mediated cell death. In conclusion these findings underscore the importance of ER stress in modulating cocaine induced microglial toxicity. Understanding the link between ER stress, oxidative stress and apoptosis could lead to the development of therapeutic strategies targeting cocaine-mediated microglial death/dysfunction.

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The Alterations in Mitochondrial DNA Copy Number and Nuclear-Encoded Mitochondrial Genes in Rat Brain Structures after Cocaine Self-Administration

et al. 2016

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The repeated intake of cocaine evokes oxidative stress that is present even during drug withdrawal. Recent studies demonstrate that cocaine-induced oxidative and/or endoplasmic reticulum stress can affect mitochondrial function and dynamics as well as the expression of mitochondrial and nuclear genes. These alterations in mitochondrial function may determine synaptic and behavioral plasticity. Mitochondria and mitochondrial DNA (mtDNA) seem to play an important role in the initiation of drug addiction. We used a microarray approach to investigate the expression patterns of nuclear-encoded genes relevant for mitochondrial functions and quantitative real-time PCR assays to determine the numbers of copies of mtDNA and of mRNAs corresponding to two mitochondrial proteins in the prefrontal cortex and hippocampus of rats during early cocaine abstinence. We found a significant elevation in the copy number of mtDNA and concomitant increased expression of mitochondrial genes. Moreover, microarray analysis revealed changes in the transcription of nuclear genes engaged in mtDNA replication, nucleoid formation, the oxidative phosphorylation pathway, and mitochondrial fission and fusion. Finally, we observed the upregulation of endoplasmic reticulum stress-induced genes. Cocaine self-administration influences the expression of both nuclear and mitochondrial genes as well as mtDNA replication. To determine whether these alterations serve as compensatory mechanisms to help maintain normal level of ATP production, further studies are necessary.Electronic supplementary materialThe online version of this article (doi:10.1007/s12035-016-0153-3) contains supplementary material, which is available to authorized users.

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Activation of c-Jun N-terminal kinase is required for the regulation of endoplasmic reticulum stress response in the rat dorsal striatum following repeated cocaine administration

Cited by 16 publications

References 20 publications

Cocaine challenge increases the expression of immunoglobulin heavy chain binding protein in the rat nucleus accumbens

Cocaine challenge increases the expression of immunoglobulin heavy chain binding protein in the rat nucleus accumbens

Role of Endoplasmic Reticulum (ER) Stress in Cocaine-Induced Microglial Cell Death

The Alterations in Mitochondrial DNA Copy Number and Nuclear-Encoded Mitochondrial Genes in Rat Brain Structures after Cocaine Self-Administration

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