Morphine induces short-lived changes in G-protein gene expression in rat prefrontal cortex

Kaewsuk, Sukit; Hutamekalin, Pilaiwan; Ketterman, Albert J.; Khotchabhakdi, Naiphinich; Govitrapong, Piyarat; Casalotti, Stefano O.

doi:10.1016/s0014-2999(00)00768-8

Cited by 23 publications

(15 citation statements)

References 21 publications

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“…Causes of the regional differences in G protein activation between FrA and PrL are likely to involve multiple mechanisms. For example, morphine increases G αi1 and G αi2 mRNA levels in PFC, which could increase the pool of available G proteins (Kaewsuk et al, 2001). Alternatively, the FrA may possess more opioid receptors than the PrL.…”

Section: Discussionmentioning

confidence: 99%

G proteins in rat prefrontal cortex (PFC) are differentially activated as a function of oxygen status and PFC region

Hambrecht

Vlisides

Row

et al. 2009

Journal of Chemical Neuroanatomy

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This study tested the hypothesis that activation of guanine nucleotide binding (G) proteins in rat prefrontal cortex (PFC) is altered by hypoxia. G protein activation by the cholinergic agonist carbachol and the opioid agonist DAMGO was quantified using [ 35 S]GTPγS autoradiography. G proteins were expressed as nCi/g tissue in the PFC of 18 rats exposed for 14 consecutive days to sustained hypoxia (10 % O 2 ), intermittent hypoxia (10 % and 21 % O 2 alternating every 90 s), or room air (21 % O 2 ). Relative to basal levels of G protein activation, carbachol and DAMGO increased G protein activation by approximately 70 % across all oxygen concentrations. Compared to the room air condition, sustained hypoxia caused a significant increase in G protein activation in frontal association (FrA) region of the PFC. Region-specific comparisons revealed that intermittent and sustained hypoxia caused greater DAMGO-stimulated G protein activation in the FrA than in the PrL. The data show for the first time that hypoxia increased G protein activation in PFC. The results suggest the potential for hypoxia-induced enhancements in G protein activation to alter PFC function.

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Section: Discussionmentioning

confidence: 99%

G proteins in rat prefrontal cortex (PFC) are differentially activated as a function of oxygen status and PFC region

Hambrecht

Vlisides

Row

et al. 2009

Journal of Chemical Neuroanatomy

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“…Adaptations in G proteins and cAMP system in numerous brain regions known to be involved in the classic effects of opiates, including the striatum, have been described (Kaewsuk et al, 2001;Matsuoka et al, 1994;Self et al, 1995;Selley et al, 1997). The modulation of transcription factors (CREB, DFosB) after chronic morphine treatment has been described (Lane Ladd et al, 1997;Maldonado et al, 1996).…”

Section: Discussionmentioning

confidence: 99%

“…Acute morphine administration induces modification of the expression of genes involved in processes as diverse as signal transduction coupled to m opioid receptors (Fan et al, 2002(Fan et al, , 2003Kaewsuk et al, 2001;Przewlocka et al, 1994), transcription factors (ErdtmannVourliotis et al, 1998;Kelz et al, 1999), and calcium binding proteins (Tirumalai and Howells, 1994). Interestingly, an analysis of the gene expression profile following a single injection of morphine revealed that one of the major groups of altered genes in the rat medial striatum consisted of cytoskeleton-related proteins (Loguinov et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Cytoskeletal Genes Regulation by Chronic Morphine Treatment in Rat Striatum

Marie-Claire

Courtin

Roques

et al. 2004

Neuropsychopharmacol

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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.

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“…Acute administration with morphine (30 mg/kg i.p.) increases expression of GNAO gene, but decreases expression of the GNAI1 and GNAI2 genes, while a chronic escalating treatment regimen (10-50 mg/kg i.p., twice daily for 2 weeks) results in increased expression levels of GNAI1 and GNAI2 genes with no change in GNAO levels (Kaewsuk et al, 2001). Although prefrontal adenylate cyclase activity was not assessed in this study, this phenomenon was suggested to be a neuronal adaptation in response to the duration of morphine treatment involved in some aspect of morphine tolerance and dependence, similar to the sort of changes previously observed in the locus coeruleus (Nestler et al, 1989).…”

Section: Drugs Of Abuse and Gα Subunitsmentioning

confidence: 99%

Alterations in the levels of heterotrimeric G protein subunits induced by psychostimulants, opiates, barbiturates, and ethanol: Implications for drug dependence, tolerance, and withdrawal

Kitanaka

Hall

et al. 2008

Synapse

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Neuronal adaptations have been found to occur in multiple brain regions after chronic intake of abused drugs, and are therefore thought to underlie drug dependence, tolerance, and withdrawal. Pathophysiological changes in drug responsiveness as well as behavioral sequelae of chronic drug exposure are thought to depend largely upon the altered state of heterotrimeric GTP binding protein (G protein)-coupled receptor (GPCR)-G protein interactions. Responsiveness of GPCR-related intracellular signaling systems to drugs of abuse is heterogeneous, depending on the types of intracellular effectors to which the specific Gα protein subtypes are coupled and GPCR-G protein coupling efficiency, factors influenced by the class of drug, expression levels of G protein subunits, and drug treatment regimens. To enhance understanding of the molecular mechanisms that underlie the development of pathophysiological states resulting from chronic intake of abused drugs, this review focuses on alterations in the expression levels of G protein subunits induced by various drugs of abuse. Changes in these mechanisms appear to be specific to particular drugs of abuse, and specific conditions of drug treatment.

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Morphine induces short-lived changes in G-protein gene expression in rat prefrontal cortex

Cited by 23 publications

References 21 publications

G proteins in rat prefrontal cortex (PFC) are differentially activated as a function of oxygen status and PFC region

G proteins in rat prefrontal cortex (PFC) are differentially activated as a function of oxygen status and PFC region

Cytoskeletal Genes Regulation by Chronic Morphine Treatment in Rat Striatum

Alterations in the levels of heterotrimeric G protein subunits induced by psychostimulants, opiates, barbiturates, and ethanol: Implications for drug dependence, tolerance, and withdrawal

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