A robust increase in expression of arc gene, an effector immediate early gene, in the rat brain after acute and chronic methamphetamine administration

Kodama, Masafumi; Akiyama, Kazufumi; Ujike, Hiroshi; Shimizu, Yoshio; Tanaka, Yuji; Kuroda, Shigetoshi

doi:10.1016/s0006-8993(98)00349-7

Cited by 68 publications

(52 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Chronic morphine produced a significant increase in the mRNA and protein levels of Arc in rat striatum. The modulation of this protein in different rat brain structures by several drugs of abuse has been previously described (Ammon et al, 2003;Fosnaugh et al, 1995;Freeman et al, 2002;Kodama et al, 1998;Tan et al, 2000). The exact function of Arc is unknown but its induction and localization in dendrites and soma (Steward and Worley, 2001;Wallace et al, 1998) led to the hypothesis of its involvement in cytoskeletal rearrangements during the process of synaptic plasticity (Lyford et al, 1995).…”

Section: Discussionmentioning

confidence: 94%

Cytoskeletal Genes Regulation by Chronic Morphine Treatment in Rat Striatum

Marie-Claire

Courtin

Roques

et al. 2004

Neuropsychopharmacol

View full text Add to dashboard Cite

It has been previously suggested that morphine can regulate the expression and function of some proteins of the cytoskeleton. In the present study, we used real-time quantitative polymerase chain reaction to examine the effects of chronic morphine administration, in rat striatum, on 14 proteins involved in microtubule polymerization and stabilization, intracellular trafficking, and serving as markers of neuronal growth and degeneration. Chronic morphine treatment led to modulation of the mRNA level of seven of the 14 genes tested. Glial fibrillary acidic protein (Gfap) and activity-regulated cytoskeleton-associated protein (Arc) mRNA were upregulated, while growth associated protein (Gap43), clathrin heavy chain (Cltc), a-tubulin, Tau, and stathmin were downregulated. In order to determine if the regulation of an mRNA correlates with a modulation of the expression of the corresponding protein, immunoblot analyses were performed. With the exception of Gap43, the levels of Cltc, Gfap, Tau, stathmin, and a-tubulin proteins were found to be in good agreement with those from mRNA quantification. These results demonstrate that neuroadaptation to chronic morphine administration in rat striatum implies modifications of the expression pattern of several genes and proteins of the cytoskeleton and cytoskeletonassociated components.

show abstract

Section: Discussionmentioning

confidence: 94%

Cytoskeletal Genes Regulation by Chronic Morphine Treatment in Rat Striatum

Marie-Claire

Courtin

Roques

et al. 2004

Neuropsychopharmacol

View full text Add to dashboard Cite

show abstract

“…Indeed, for the study of DA neurotoxicity and other neuropsychiatric conditions involving DA neurons, we have recently developed "DA" and "neuronal" microarrays and have used them to identify a number of mRNA changes in the context of METHinduced DA neurotoxicity (Barrett et al, 2001). However, whether any of the gene expression changes that we and others (Merchant et al, 1994;Smith and McGinty, 1994;Wang and McGinty, 1995;Sheng et al, 1996;Badiani et al, 1998Badiani et al, , 1999Kodama et al, 1998;Jayanthi et al, 1999;Cadet et al, 2001) have identified after METH administration are directly linked to the neurotoxic process has yet to be established.…”

Section: Abstract: Amphetamines; Neurotoxicity; Dopamine; Neurodegenmentioning

confidence: 93%

Changes in Gene Expression Linked to Methamphetamine-Induced Dopaminergic Neurotoxicity

Xie¹,

Tong²,

Barrett

et al. 2002

J. Neurosci.

View full text Add to dashboard Cite

The purpose of these studies was to examine the role of gene expression in methamphetamine (METH)-induced dopamine (DA) neurotoxicity. First, the effects of the mRNA synthesis inhibitor, actinomycin-D, and the protein synthesis inhibitor, cycloheximide, were examined. Both agents afforded complete protection against METH-induced DA neurotoxicity and did so independently of effects on core temperature, DA transporter function, or METH brain levels, suggesting that gene transcription and mRNA translation play a role in METH neurotoxicity. Next, microarray technology, in combination with an experimental approach designed to facilitate recognition of relevant gene expression patterns, was used to identify gene products linked to METH-induced DA neurotoxicity. This led to the identification of several genes in the ventral midbrain associated with the neurotoxic process, including genes for energy metabolism [cytochrome c oxidase subunit 1 (COX1), reduced nicotinamide adenine dinucleotide ubiquinone oxidoreductase chain 2, and phosphoglycerate mutase B], ion regulation (members of sodium/hydrogen exchanger and sodium/bile acid cotransporter family), signal transduction (adenylyl cyclase III), and cell differentiation and degeneration (N-myc downstreamregulated gene 3 and tau protein). Of these differentially expressed genes, we elected to further examine the increase in COX1 expression, because of data implicating energy utilization in METH neurotoxicity and the known role of COX1 in energy metabolism. On the basis of time course studies, Northern blot analyses, in situ hybridization results, and temperature studies, we now report that increased COX1 expression in the ventral midbrain is linked to METH-induced DA neuronal injury. The precise role of COX1 and other genes in METH neurotoxicity remains to be elucidated. Key words: amphetamines; neurotoxicity; dopamine; neurodegeneration; cytochrome c oxidase; microarrayDespite considerable investigation (Gibb et al., 1994;Lew et al., 1997), the mechanisms underlying the neurotoxic effects of methamphetamine (METH) on brain dopamine (DA) neurons remain unknown. However, a considerable body of data attests to the importance of DA transporter (DAT) function and temperature. The essential role of the DAT in METH-induced DA neurotoxicity has been demonstrated by the observation that DAT inhibitors afford complete neuroprotection (Ricaurte et al., 1984; Marek et al., 1990a,b;Pu et al., 1994) and the finding that DAT knock-out mice are insensitive to METH neurotoxicity (Fumagalli et al., 1998). The importance of temperature has been documented by studies demonstrating that decreases in core temperature protect against METH neurotoxicity, whereas increases in core temperature exacerbate the toxicity (Bowyer et al., 1994;Miller and O'Callaghan, 1994;Albers and Sonsalla, 1995;Ali et al., 1996). Furthermore, there is evidence that at least part of the effect of temperature on METH neurotoxicity is mediated at the level of the DAT (Xie et al., 2000). More recent studies have also i...

show abstract

“…In situ hybridization analysis was conducted using 35 Slabeled oligonucleotide probes as previously described with some minor modifications (Kodama et al, 1998). Coronal sections from sham-and ECS-treated animals, two per animal, were processed at the same time.…”

Section: In Situ Hybridizationmentioning

confidence: 99%

Electroconvulsive Seizures Increase the Expression of MAP Kinase Phosphatases in Limbic Regions of Rat Brain

Kodama

Russell

Duman

2004

Neuropsychopharmacol

Self Cite

View full text Add to dashboard Cite

The mitogen-activated protein (MAP) kinase cascades regulate a variety of cellular activities, including cell growth, proliferation, and apoptosis, and are reported to play a role in the actions of antidepressant treatment. There are a number of different classes of protein phosphatases that could influence the MAP kinase cascade. One of these, the MAP kinase phosphatase (MKP) family, is known to play a key role in dephosphorylation of activated MAP kinase. In the present study, we analyzed the expression of the MKP1, MKP2, and MKP3 isoforms in rat brain after electroconvulsive seizure (ECS), considered the most effective treatment for depression. In situ hybridization analysis demonstrates that ECS differentially regulates the expression of the MKP isoforms. Expression of MKP1 mRNA is robustly increased by acute ECS in the major cell layers of the hippocampus, including the dentate gyrus granule cell layer and the CA1 and CA3 pyramidal cell layers. In contrast, MKP2 is induced mainly in the dentate gyrus and MKP3 is preferentially increased in the CA1 and CA3 cell layers. In the prefrontal cortex, all three MKP isoforms are upregulated by acute ECS administration. Chronic ECS resulted in a similar pattern of induction for each of the MKP subtypes, demonstrating that there is little or no desensitization of the response to repeated ECS. The induction of MKP expression serves as negative feedback control for the MAP kinase cascades. Upregulation of MKP expression could dampen the actions of ECS, indicating that blockade of the MKPs could enhance the actions of antidepressant treatment.

show abstract

A robust increase in expression of arc gene, an effector immediate early gene, in the rat brain after acute and chronic methamphetamine administration

Cited by 68 publications

References 27 publications

Cytoskeletal Genes Regulation by Chronic Morphine Treatment in Rat Striatum

Cytoskeletal Genes Regulation by Chronic Morphine Treatment in Rat Striatum

Changes in Gene Expression Linked to Methamphetamine-Induced Dopaminergic Neurotoxicity

Electroconvulsive Seizures Increase the Expression of MAP Kinase Phosphatases in Limbic Regions of Rat Brain

Contact Info

Product

Resources

About