Novelty-induced increased expression of immediate-early genes c-fos and arg 3.1 in the mouse brain

Montag-Sallaz, M.; Welzl, Hans; Kuhl, Dietmar; Montag, Dirk; Schachner, Melitta

doi:10.1002/(sici)1097-4695(19990205)38:2<234::aid-neu6>3.0.co;2-g

Cited by 130 publications

(37 citation statements)

References 36 publications

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“…Studies over the last decade have exploited the rapid expression of immediate early genes such as Arc , c-fos , zif268 , and homer1a to map neuronal populations and circuits engaged in distinct forms of learning (Guzowski et al 1999; Montag et al 1999; Vazdarjanova et al 2002; Kelly and Deadwyler 2003; Montag-Sallaz and Montag 2003; Vazdarjanova and Guzowski 2004; Gusev et al 2005; Kubik et al 2007; Soule et al 2008). Work of Vazdarjanova and Guzowski (2004) further established a tight link between Arc transcription and neural activity specifically associated with information processing in hippocampal subfields.…”

Section: Arc and Memory Consolidationmentioning

confidence: 99%

The Arc of synaptic memory

et al. 2009

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The immediate early gene Arc is emerging as a versatile, finely tuned system capable of coupling changes in neuronal activity patterns to synaptic plasticity, thereby optimizing information storage in the nervous system. Here, we attempt to overview the Arc system spanning from transcriptional regulation of the Arc gene, to dendritic transport, metabolism, and translation of Arc mRNA, to post-translational modification, localization, and degradation of Arc protein. Within this framework we discuss the function of Arc in regulation of actin cytoskeletal dynamics underlying consolidation of long-term potentiation (LTP) and regulation of AMPA-type glutamate receptor endocytosis underlying long-term depression (LTD) and homeostatic plasticity. Behaviorally, Arc has a key role in consolidation of explicit and implicit forms of memory, with recent work implicating Arc in adaptation to stress as well as maladaptive plasticity connected to drug addiction. Arc holds considerable promise as a “master regulator” of protein synthesis-dependent forms of synaptic plasticity, but the mechanisms that modulate and switch Arc function are only beginning to be elucidated.

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Section: Arc and Memory Consolidationmentioning

confidence: 99%

The Arc of synaptic memory

et al. 2009

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“…Because c-Fos has been shown to be an IEG that is upregulated after behavioral training (Montag-Sallaz et al, 1999), we also included c-Fos as a positive control in the quantitative PCR assay. Similar to Tbr1 mRNA, we found that the c-Fos expression levels in the lateral amygdala, insular cortex, and ventral hippocampus were upregulated at 2 h but returned to a level comparable to that of the control 24 h after CTA training ( Figure 4E ).…”

Section: Resultsmentioning

confidence: 99%

Neuronal excitation upregulates Tbr1, a high-confidence risk gene of autism, mediating Grin2b expression in the adult brain

Chuang

Huang

Hsueh

2014

Front. Cell. Neurosci.

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The activity-regulated gene expression of transcription factors is required for neural plasticity and function in response to neuronal stimulation. T-brain-1 (TBR1), a critical neuron-specific transcription factor for forebrain development, has been recognized as a high-confidence risk gene for autism spectrum disorders. Here, we show that in addition to its role in brain development, Tbr1 responds to neuronal activation and further modulates the Grin2b expression in adult brains and mature neurons. The expression levels of Tbr1 were investigated using both immunostaining and quantitative reverse transcription polymerase chain reaction (RT-PCR) analyses. We found that the mRNA and protein expression levels of Tbr1 are induced by excitatory synaptic transmission driven by bicuculline or glutamate treatment in cultured mature neurons. The upregulation of Tbr1 expression requires the activation of both α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) and N-methyl-D-aspartate (NMDA) receptors. Furthermore, behavioral training triggers Tbr1 induction in the adult mouse brain. The elevation of Tbr1 expression is associated with Grin2b upregulation in both mature neurons and adult brains. Using Tbr1-deficient neurons, we further demonstrated that TBR1 is required for the induction of Grin2b upon neuronal activation. Taken together with the previous studies showing that TBR1 binds the Grin2b promoter and controls expression of luciferase reporter driven by Grin2b promoter, the evidence suggests that TBR1 directly controls Grin2b expression in mature neurons. We also found that the addition of the calcium/calmodulin-dependent protein kinase II (CaMKII) antagonist KN-93, but not the calcium-dependent phosphatase calcineurin antagonist cyclosporin A, to cultured mature neurons noticeably inhibited Tbr1 induction, indicating that neuronal activation upregulates Tbr1 expression in a CaMKII-dependent manner. In conclusion, our study suggests that Tbr1 plays an important role in adult mouse brains in response to neuronal activation to modulate the activity-regulated gene transcription required for neural plasticity.

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“…Similarly with our findings, previous studies also suggested the distinct regulation of Arc and c-fos expression. For example, experience of a novel taste led to an increase of c-fos mRNA expression in the amygdala and ACC and an increase of Arc mRNA expression in the hippocampus and ACC in mice [13]. Numerous studies have investigated the molecular mechanisms for the transcriptional regulation of the c-fos and Arc genes at the promoter level, and demonstrated the distinct structures of their promoters, regulatory elements, and transcription factors binding to these elements [16,80,81].…”

Section: Discussionmentioning

confidence: 99%

Induction and requirement of gene expression in the anterior cingulate cortex and medial prefrontal cortex for the consolidation of inhibitory avoidance memory

2011

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BackgroundMemory consolidation is a process to stabilize short-term memory, generating long-term memory. A critical biochemical feature of memory consolidation is a requirement for gene expression. Previous studies have shown that fear memories are consolidated through the activation of gene expression in the amygdala and hippocampus, indicating essential roles of these brain regions in memory formation. However, it is still poorly understood whether gene expression in brain regions other than the amygdala/hippocampus is required for the consolidation of fear memory; however, several brain regions are known to play modulatory roles in fear memory formation.ResultsTo further understand the mechanisms underlying the formation of fear memory, we first identified brain regions where gene expression is activated after learning inhibitory avoidance (IA) by analyzing the expression of the immediately early genes c-fos and Arc as markers. Similarly with previous findings, the induction of c-fos and Arc expression was observed in the amygdala and hippocampus. Interestingly, we also observed the induction of c-fos and Arc expression in the medial prefrontal cortex (mPFC: prelimbic (PL) and infralimbic (IL) regions) and Arc expression in the anterior cingulate cortex (ACC). We next examined the roles of these brain regions in the consolidation of IA memory. Consistent with previous findings, inhibiting protein synthesis in the hippocampus blocked the consolidation of IA memory. More importantly, inhibition in the mPFC or ACC also blocked the formation of IA memory.ConclusionOur observations indicated that the formation of IA memory requires gene expression in the ACC and mPFC as well as in the amygdala and hippocampus, suggesting essential roles of the ACC and mPFC in IA memory formation.

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Novelty-induced increased expression of immediate-early genes c-fos and arg 3.1 in the mouse brain

Cited by 130 publications

References 36 publications

The Arc of synaptic memory

The Arc of synaptic memory

Neuronal excitation upregulates Tbr1, a high-confidence risk gene of autism, mediating Grin2b expression in the adult brain

Induction and requirement of gene expression in the anterior cingulate cortex and medial prefrontal cortex for the consolidation of inhibitory avoidance memory

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