Identification of genes co‐upregulated with <i>Arc</i> during BDNF‐induced long‐term potentiation in adult rat dentate gyrus <i>in vivo</i>

Wibrand, Karin; Messaoudi, Elhoucine; Håvik, Bjarte; Steenslid, Vibeke; Løvlie, Roger; Steen, Vidar M.; Bramham, Clive R.

doi:10.1111/j.1460-9568.2006.04687.x

Cited by 134 publications

(124 citation statements)

References 82 publications

(112 reference statements)

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“…A panel of genes that are co-upregulated with Arc during BDNF-LTP and HFS-LTP was recently identified (Wibrand et al, 2006). Several of these genes [Narp (neuronal activity regulated pentraxin), neuritin, Nedd4 WW-binding protein-4) have functions in AMPAR clustering, excitatory synaptogenesis, and axonal guidance.…”

Section: Discussionmentioning

confidence: 99%

Sustained Arc/Arg3.1 Synthesis Controls Long-Term Potentiation Consolidation through Regulation of Local Actin Polymerization in the Dentate GyrusIn Vivo

Messaoudi¹,

Kanhema²,

Soulé³

et al. 2007

J. Neurosci.

418

463

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New gene expression is necessary for long-term potentiation (LTP) consolidation, yet roles for specific activity-induced mRNAs have not been defined. Here we probed the dynamic function of activity-induced Arc (activity-regulated cytoskeletal-associated protein)/Arg3.1 (activity-regulated gene 3.1 protein homolog) mRNA using brief, local infusions of antisense (AS) oligodeoxynucleotides at multiple time points during dentate gyrus LTP in vivo. Surprisingly, early Arc synthesis is necessary for early expression of LTP, whereas sustained synthesis is required to generate stably modified synapses. AS application 2 h after LTP induction results in a rapid and permanent reversal of LTP. This reversal is associated with rapid knockdown of upregulated Arc, dephosphorylation of actin depolymerization factor/cofilin, and loss of nascent filamentous actin (F-actin) at synaptic sites. Infusion of the F-actin stabilizing drug jasplakinolide during LTP maintenance blocks the ability of AS to reverse LTP. These results couple activity-induced expression of Arc to expansion of the actin cytoskeleton underlying enduring LTP. Furthermore, Arc synthesis is required for both the induction and consolidation of LTP elicited by local BDNF infusion, thus identifying Arc as a key molecular effector of BDNF in synaptic plasticity.

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Section: Discussionmentioning

confidence: 99%

Sustained Arc/Arg3.1 Synthesis Controls Long-Term Potentiation Consolidation through Regulation of Local Actin Polymerization in the Dentate GyrusIn Vivo

Messaoudi¹,

Kanhema²,

Soulé³

et al. 2007

J. Neurosci.

418

463

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“…Dclk1-long, a product of the alternative splice variants of Dclk1, is a microtubule-associated active protein kinase expressed in neurites (Burgess and Reiner, 2000). Carp (Ania-4) has been reported to be involved in apoptosis and tubulin polymerization in vitro (Schenk et al, 2007) and in seizures and long-term potentiation in vivo (Schenk et al, 2011;Vreugdenhil et al, 1999;Wibrand et al, 2006). Thus, the DCLK1 proteins might direct the latent process of neural cell differentiation by controlling tubulin formation or by modulating cell viability and subsequent synaptic plasticity (Kawaai et al, 2010;Shu et al, 2006;Vreugdenhil et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

Latent process genes for cell differentiation are common decoders of neurite extension length

Watanabe

Akimoto

Yugi

et al. 2012

Journal of Cell Science

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SummaryA latent process involving signal transduction and gene expression is needed as a preparation step for cellular function. We previously found that nerve growth factor (NGF)-induced cell differentiation has a latent process, which is dependent on ERK activity and gene expression and required for subsequent neurite extension. A latent process can be considered as a preparation step that decodes extracellular stimulus information into cellular functions; however, molecular mechanisms of this process remain unknown. We identified Metrnl, Dclk1 and Serpinb1a as genes that are induced during the latent process (LP) with distinct temporal expression profiles and are required for subsequent neurite extension in PC12 cells. The LP genes showed distinct dependency on the duration of ERK activity, and they were also induced during the latent process of PACAP-and forskolin-induced cell differentiation. Regardless of neurotrophic factors, expression levels of the LP genes during the latent process (0-12 hours), but not phosphorylation levels of ERK, always correlated with subsequent neurite extension length (12-24 hours). Overexpression of all LP genes together, but not of each gene separately, enhanced NGF-induced neurite extension. The LP gene products showed distinct spatial localization. Thus, the LP genes appear to be the common decoders for neurite extension length regardless of neurotrophic factors, and they might function in distinct temporal and spatial manners during the latent process. Our findings provide molecular insight into the physiological meaning of the latent process as the preparation step for decoding information for future phenotypic change.

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“…BDNF promotes synaptic plasticity and synaptic consolidation that are dependent upon the transcription and translation of arc (Kang and Schuman 1996;Guzowski et al 2001;Messaoudi et al 2002;Bramham and Messaoudi 2005;Soule et al 2006;Wibrand et al 2006). Thus, an increase in bdnf mRNA in the cortex may drive the arc response by initiating translation of newly synthesized arc mRNA in activated dendritic spines (Yin et al 2002;Ying et al 2002).…”

Section: Functional Significance Of Gene Expression Changesmentioning

confidence: 99%

Relapse to cocaine seeking increases activity-regulated gene expression differentially in the prefrontal cortex of abstinent rats

et al. 2008

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Rationale-Alterations in the activity of the prefrontal and orbitofrontal cortices of cocaine addicts have been linked with re-exposure to cocaine-associated stimuli. Objectives Using an animal model of relapse to cocaine seeking, the present study investigated the expression patterns of four different activity-regulated genes within prefrontal cortical brain regions after 22 h or 15 days of abstinence during context-induced relapse.Materials and methods-Rats self-administered cocaine or received yoked-saline for 2 h/day for 10 days followed by 22 h or 2 weeks of abstinence when they were re-exposed to the selfadministration chamber with or without levers available to press for 1 h. Brains were harvested and sections through the prefrontal cortex were processed for in situ hybridization using radioactive oligonucleotide probes encoding c-fos, zif/268, arc, and bdnf.Results-Re-exposure to the chamber in which rats previously self-administered cocaine but not saline, regardless of lever availability, increased the expression of all genes in the medial prefrontal and orbitofrontal cortices at both time points with one exception: bdnf mRNA was significantly increased in the medial prefrontal cortex at 22 h only if levers previously associated with cocaine delivery were available to press. Furthermore, re-exposure of rats to the chambers in which they received yoked saline enhanced both zif/268 and arc expression selectively in the orbito-frontal cortex after 15 days of abstinence.Correspondence to: J. F. McGinty. HHS Public AccessAuthor manuscript Psychopharmacology (Berl). Author manuscript; available in PMC 2017 May 22. Author Manuscript Author ManuscriptAuthor Manuscript Author ManuscriptConclusions-These results support convergent evidence that cocaine-induced changes in the prefrontal cortex are important in regulating drug seeking following abstinence and may provide additional insight into the molecular mechanisms involved in these processes. KeywordsAddiction; Arc; BDNF; c-fos; Relapse; zif/268; Self-administration; Abstinence; ExtinctionRelapse to drug seeking and taking in addicted humans is often triggered by re-exposure to environmental cues previously associated with the drug (Ehrman et al. 1992). Similarly, in animal studies, during chronic drug self-administration, the drug-paired environment acquires conditioned reinforcing properties that trigger drug-seeking behavior upon reexposure to the context following forced abstinence (Crombag and Shaham 2002;Fuchs et al. 2005Fuchs et al. , 2006. Thus, like other forms of learning, relapse to drug-seeking involves the formation and retrieval of instrumental memories (Hyman 2005). A major question in addiction research is whether the neural substrates underlying drug-seeking involve the same cell signaling and synaptic plasticity processes within the same brain regions as those implicated in other forms of reward learning and memory (Berke and Hyman 2000;Hyman and Malenka 2001;Nestler 2001).The inhibitory control functions of the prefrontal cortical ...

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Identification of genes co‐upregulated with Arc during BDNF‐induced long‐term potentiation in adult rat dentate gyrus in vivo

Cited by 134 publications

References 82 publications

Sustained Arc/Arg3.1 Synthesis Controls Long-Term Potentiation Consolidation through Regulation of Local Actin Polymerization in the Dentate GyrusIn Vivo

Sustained Arc/Arg3.1 Synthesis Controls Long-Term Potentiation Consolidation through Regulation of Local Actin Polymerization in the Dentate GyrusIn Vivo

Latent process genes for cell differentiation are common decoders of neurite extension length

Relapse to cocaine seeking increases activity-regulated gene expression differentially in the prefrontal cortex of abstinent rats

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