Inhibition of <i>Period1</i> Gene Attenuates the Morphine-Induced ERK-CREB Activation in Frontal Cortex, Hippocampus, and Striatum in Mice

Li, Suxia; Wang, Zhengrong; Li, Jing; Peng, Zugui; Wei, Zhou; Zhou, Mei; Lü, Lin

doi:10.1080/00952990802308197

Cited by 17 publications

(8 citation statements)

References 23 publications

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“…These changes are in good agreement with current models indicating that Rev-erba acts as a potent repressor of Cry1 expression and that Cry1 works as a negative regulator of Per1 expression (Etchegaray et al, 2003). The potential behavioral relevance of these changes in Per1 expression is highlighted by studies showing that both mice and Drosophila mutants, lacking, respectively, Per1 or Per, failed to show sensitization to cocaine (Abarca et al, 2002;Andretic et al, 1999), and the reduction of Per1 activity in mice by DNAzyme led to a reduction in CPP for morphine (Li et al, 2008). The mechanisms by which circadian clock genes regulate addictive behavior remain elusive (Perreau-Lenz et al, 2007), but probably involve their regulatory function on dopamine receptor responsiveness (Andretic and Hirsh, 2000).…”

Section: Discussionsupporting

confidence: 64%

Selective Boosting of Transcriptional and Behavioral Responses to Drugs of Abuse by Histone Deacetylase Inhibition

Sanchis‐Segura

López‐Atalaya

Barco

2009

Neuropsychopharmacol

121

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Histone acetylation and other modifications of the chromatin are important regulators of gene expression and, consequently, may contribute to drug-induced behaviors and neuroplasticity. Earlier studies have shown that a reduction in histone deacetylase (HDAC) activity results in the enhancement of some psychostimulant-induced behaviors. In this study, we extend those seminal findings by showing that the administration of the HDAC inhibitor sodium butyrate enhances morphine-induced locomotor sensitization and conditioned place preference. In contrast, this compound has no effects on the development of morphine tolerance and dependence. Similar effects were observed for cocaine and ethanol-induced behaviors. These behavioral changes were accompanied by a selective boosting of a component of the transcriptional program activated by chronic morphine administration that included circadian clock genes and other genes relevant to addictive behavior. Our results support a specific function for histone acetylation and the epigenetic modulation of transcription at a reduced number of biologically relevant loci on non-homeostatic, long-lasting, drug-induced behavioral plasticity.

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Section: Discussionsupporting

confidence: 64%

Selective Boosting of Transcriptional and Behavioral Responses to Drugs of Abuse by Histone Deacetylase Inhibition

Sanchis‐Segura

López‐Atalaya

Barco

2009

Neuropsychopharmacol

121

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“…We found that chronic morphine exposure increased p-ERK and p-CREB expression in the vHip and mPFC following D1R activation. These results are consistent with a previous study [29]. Our previous study has revealed that these protein levels in Hip are positively correlated with D1R activation during memory processes [24].…”

Section: Discussionsupporting

confidence: 94%

Opiate-associated contextual memory formation and retrieval are differentially modulated by dopamine D1 and D2 signaling in hippocampal–prefrontal connectivity

Wang

Zhang

Cui

et al. 2018

Neuropsychopharmacol

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Contextual memory driven by abused drugs such as opiates has a central role in maintenance and relapse of drug-taking behaviors. Although dopamine (DA) signaling favors memory storage and retrieval via regulation of hippocampal-prefrontal connectivity, its role in modulating opiate-associated contextual memory is largely unknown. Here, we report roles of DA signaling within the hippocampal-prefrontal circuit for opiate-related memories. Combining-conditioned place preference (CPP) with molecular analyses, we investigated the DA D1 receptor (D1R) and extracellular signal-regulated kinase (ERK)-cAMP-response element binding protein (CREB) signaling, as well as DA D2 receptor (D2R) and protein kinase B (PKB or Akt)/glycogen synthase kinase 3 (GSK3) signaling in the ventral hippocampus (vHip) and medial prefrontal cortex (mPFC) during the formation of opiate-related associative memories. Morphine-CPP acquisition increased the activity of the D1R-ERK-CREB pathway in both the vHip and mPFC. Morphine-CPP reinstatement was associated with the D2R-mediated hyperactive GSK3 via Akt inhibition in the vHip and PFC. Furthermore, integrated D1R-ERK-CREB and D2R-Akt-GSK3 pathways in the vHip-mPFC circuit are required for the acquisition and retrieval of the morphine contextual memory, respectively. Moreover, blockage of D1R or D2R signaling could alleviate normal Hip-dependent spatial memory. These results suggest that D1R and D2R signaling are differentially involved in the acquisition and retrieval of morphine contextual memory, and DA signaling in the vHip-mPFC connection contributes to morphine-associated and normal memory, largely depending on opiate exposure states.

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“…Interestingly, the results of our study demonstrated that ERK1/2 and CREB protein levels in hippocampus are not changed, rather pERK1/2 and pCREB protein levels in the hippocampus are up-regulated markedly in both the acquisition and maintenance of morphine conditioned place preference memory. These results are consistent with prior reports that the ERK-CREB pathway is involved in chronic morphine associated memory 38 39 , especially in the mechanism for the reconsolidation of drug addiction memory 40 .…”

Section: Discussionsupporting

confidence: 93%

RACK1 promotes maintenance of morphine-associated memory via activation of an ERK-CREB dependent pathway in hippocampus

Liu

Zhu

Zhou

et al. 2016

Sci Rep

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Existence of long-term drug-associated memories may be a crucial factor in drug cravings and relapse. RACK1 plays a critical role in morphine-induced reward. In the present study, we used conditioned place preference (CPP) to assess the acquisition and maintenance of morphine conditioned place preference memory. The hippocampal protein level of RACK1 and synaptic quantitation were evaluated by Western blotting, immunohistochemistry and electron microscopy, respectively. Additionally, shRACK1 (shGnb2l1) was used to silence RACK1 in vivo to evaluate the role and the underlying mechanism of RACK1 in maintenance of morphine CPP memory. We found that morphine induced CPP was maintained for at least 7 days after the last morphine treatment, which indicated a positive correlation with hippocampal RACK1 level, and was accompanied simultaneously by increases in the synapse density and hippocampal expression of synaptophysin (SYP), phosphorylation of extracellular signal-regulated kinase1/2 (pERK1/2) and the phosphorylation of cyclic adenosine monophosphate response element-binding (pCREB). ShGnb2l1 icv injection significantly suppressed the expression of all above proteins, decreased the synapse density in the hippocampus and attenuated the acquisition and maintenance of morphine CPP. Our present study highlights that RACK1 plays an important role in the maintenance of morphine CPP, likely via activation of ERK-CREB pathway in hippocampus.

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Inhibition of Period1 Gene Attenuates the Morphine-Induced ERK-CREB Activation in Frontal Cortex, Hippocampus, and Striatum in Mice

Abstract: Our results indicated that per1 plays an important role in morphine reward, and ERK-CREB pathway was involved in the effects of per1. We suggested that per1 gene may be a potential treatment target for drug addition.

Cited by 17 publications

References 23 publications

Selective Boosting of Transcriptional and Behavioral Responses to Drugs of Abuse by Histone Deacetylase Inhibition

Selective Boosting of Transcriptional and Behavioral Responses to Drugs of Abuse by Histone Deacetylase Inhibition

Opiate-associated contextual memory formation and retrieval are differentially modulated by dopamine D1 and D2 signaling in hippocampal–prefrontal connectivity

RACK1 promotes maintenance of morphine-associated memory via activation of an ERK-CREB dependent pathway in hippocampus

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