Satoshi Kida

Tokyo University of Agriculture, Edo, Tōkyō, Japan

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Publications (78)235.03 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: CREB is a pivotal mediator of activity-regulated gene transcription that underlies memory formation and allocation. The contribution of a key CREB cofactor, CREB-regulated transcription coactivator 1 (CRTC1), has, however, remained elusive. Here we show that several constitutive kinase pathways and an activity-regulated phosphatase, calcineurin, converge to determine the nucleocytoplasmic shuttling of CRTC1. This, in turn, triggered an activity-dependent association of CRTC1 with CREB-dependent regulatory elements found on IEG promoters. Forced expression of nuclear CRTC1 in hippocampal neurons activated CREB-dependent transcription, and was sufficient to enhance contextual fear memory. Surprisingly, during contextual fear conditioning, we found evidence of nuclear recruitment of endogenous CRTC1 only in the basolateral amygdala, and not in the hippocampus. Consistently, CRTC1 knockdown in the amygdala, but not in the hippocampus, significantly attenuated fear memory. Thus, CRTC1 has a wide impact on CREB-dependent memory processes, but fine-tunes CREB output in a region-specific manner.
    10/2014; 84(1):92–106.
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    ABSTRACT: Memory retrieval is considered to have roles in memory enhancement. Recently, memory reconsolidation was suggested to reinforce or integrate new information into reactivated memory. Here, we show that reactivated inhibitory avoidance (IA) memory is enhanced through reconsolidation under conditions in which memory extinction is not induced. This memory enhancement is mediated by neurons in the amygdala, hippocampus, and medial prefrontal cortex (mPFC) through the simultaneous activation of calcineurin-induced proteasome-dependent protein degradation and cAMP responsive element binding protein-mediated gene expression. Interestingly, the amygdala is required for memory reconsolidation and enhancement, whereas the hippocampus and mPFC are required for only memory enhancement. Furthermore, memory enhancement triggered by retrieval utilizes distinct mechanisms to strengthen IA memory by additional learning that depends only on the amygdala. Our findings indicate that reconsolidation functions to strengthen the original memory and show the dynamic nature of reactivated memory through protein degradation and gene expression in multiple brain regions.DOI: http://dx.doi.org/10.7554/eLife.02736.001.
    eLife Sciences 06/2014; 3:e02736. · 8.52 Impact Factor
  • Satoshi Kida, Tatsurou Serita
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    ABSTRACT: cAMP response element-binding (CREB) has been known to be an essential transcription factor that activates the gene expression required for the formation of long-term memory (LTM) in a wide range of animal models, from nematodes to higher animals such as Aplysia, Drosophila, and rodents. In mammals, various CREB mutant mice have been developed and analyzed. These studies have shown that gain or loss of CREB function improves and impairs, respectively, the formation of LTMs, enabling us to understand the roles of CREB in the formation and enhancement of memory. In this article, the analyses conducted on CREB mutant mice are reviewed with a particular focus on learning and memory formation.
    Brain research bulletin 05/2014; · 2.97 Impact Factor
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    ABSTRACT: Adult hippocampal neurogenesis has been suggested to play modulatory roles in learning and memory. Importantly, previous studies have shown that newborn neurons in the adult hippocampus are integrated into the dentate gyrus circuit and are recruited more efficiently into the hippocampal memory trace of mice when they become 3 weeks old. Interestingly, a single high-dose treatment with the N-methyl-D-aspartate receptor antagonist memantine (MEM) has been shown to increase hippocampal neurogenesis dramatically by promoting cell proliferation. In the present study, to understand the impact of increased adult neurogenesis on memory performance, we examined the effects of a single treatment of MEM on hippocampus-dependent memory in mice. Interestingly, mice treated with MEM showed an improvement of hippocampus-dependent spatial and social recognition memories when they were trained and tested at 3~6 weeks, but not at 3 days or 4 months, after treatment with MEM. Importantly, we observed a significant positive correlation between the scores for spatial memory (probe trial in the Morris water maze task) and the number of young mature neurons (3 weeks old) in MEM-treated mice, but not saline-treated mice. We also observed that the young mature neurons generated by treatment with MEM were recruited into the trace of spatial memory similarly to those generated through endogenous neurogenesis. Taken together, our observations suggest that treatment with MEM temporally improves hippocampus-dependent memory formation and that the newborn neurons increased by treatment with MEM contribute to this improvement when they become 3 weeks old. © 2014 Wiley Periodicals, Inc.
    Hippocampus 03/2014; · 5.49 Impact Factor
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    Ken-Ichi Kato, Taku Iwamoto, Satoshi Kida
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    ABSTRACT: alphaCaMKII plays central and essential roles in long-term potentiation (LTP), learning and memory. alphaCaMKII is activated via binding with Ca2+/CaM in response to elevated Ca2+ concentration. Furthermore, prolonged increase in Ca2+ concentration leads to the auto-phosphorylation of alphaCaMKII at T286, maintaining the activation of alphaCaMKII even after Ca2+/CaM dissociation. Importantly, the active form of alphaCaMKII is thought to exhibit conformational change. In order to elucidate the relationships between the interaction of alphaCaMKII with CaM and the conformational change of alphaCaMKII, we generated molecular probes (YFP-alphaCaMKII with CFP-CaM and YFP-alphaCaMKII-CFP) and performed time-lapse imaging of the interaction with CaM and the conformational change, respectively, in living cells using FRET. The interaction of YFP-alphaCaMKII with CFP-CaM and the conformational change of YFP-alphaCaMKII-CFP were induced simultaneously in response to increased concentrations of Ca2+. Consistent with previous predictions, high levels of Ca2+ signaling maintained the conformational change of YFP-alphaCaMKII-CFP at the time when CFP-CaM was released from YFP-alphaCaMKII. These observations indicated the transfer of alphaCaMKII conformational change from CaM-dependence to CaM-independence. Furthermore, analyses using alphaCaMKII mutants showed that phosphorylation at T286 and T305/305 played positive and negative roles, respectively, during in vivo interaction with CaM and further suggested that CaM-dependent and CaM-independent conformational changed forms displays similar but distinct structures. Importantly, these structual differences between CaM-dependent and -independent forms of alphaCaMKII may exhibit differential functions for alphaCaMKII, such as interactions with other molecules required for LTP and memory. Our molecular probes could thus be used to identify therapeutic targets for cognitive disorders that are associated with the misregulation of alphaCaMKII.
    Molecular Brain 08/2013; 6(1):37. · 4.20 Impact Factor
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    ABSTRACT: CREB has been reported to be activated by injury and is commonly used as marker for pain-related plasticity changes in somatosensory pathways, including spinal dorsal horn neurons and the anterior cingulate cortex (ACC). However no evidence has been reported to support the direct role of activated CREB in injury-related behavioral sensitization (or allodynia). Here we report that genetic enhancement of CREB-mediated transcription selectively in forebrain areas enhanced behavioral responses to non-noxious stimuli after chronic inflammation (CFA model) or nerve injury. In contrast, behavioral acute responses to peripheral subcutaneous injection of formalin did not show any significant difference. Furthermore, acute pain responses to noxious thermal stimuli were also not affected. Our results thus provide direct evidence that cortical CREB-mediated transcription contributes to behavioral allodynia in animal models of chronic inflammatory or neuropathic pain.
    Molecular Pain 12/2012; 8(1):90. · 3.77 Impact Factor
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    Satoshi Kida
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    ABSTRACT: cAMP response element-binding protein (CREB), a transcription factor, has been shown to play a central role in memory formation, and its involvement in this process has been investigated using a wide range of animal models, from nematodes to higher animals. Various CREB mutant mice have been developed and investigated. Several types of mutant mice with loss of CREB function have impaired memory formation and long-term potentiation (LTP), suggesting that CREB plays essential roles in these processes. To characterize the roles of CREB in memory formation and LTP further, mutant mice displaying gain of CREB function have been generated and analyzed. Importantly, CREB-DIEDML mice and CREB-Y134F mice showed enhanced memory formation, whereas CREB-VP16 mice displayed a lowered threshold of long-lasting LTP (L-LTP) induction, strongly suggesting that CREB functions as a positive regulator of memory formation and LTP. In this review, I focus on the effects of the genetic activation of CREB in LTP and memory formation and summarize previous findings.
    Experimental neurobiology. 12/2012; 21(4):136-40.
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    ABSTRACT: Fragile X syndrome is caused by lack of fragile X mental retardation protein (FMRP) due to silencing of the FMR1 gene. The metabotropic glutamate receptors (mGluRs) in the central nervous system contribute to higher brain functions including learning/memory, mental disorders and persistent pain. The transcription factor cyclic AMP-responsive element binding protein (CREB) is involved in important neuronal functions, such as synaptic plasticity and neuronal survival. Our recent study has shown that stimulation of Group I mGluRs upregulated FMRP and activated CREB in anterior cingulate cortex (ACC), a key region for brain cognitive and executive functions, suggesting that activation of Group I mGluRs may upregulate FMRP through CREB signaling pathway. In this study, we demonstrate that CREB contributes to the regulation of FMRP by Group I mGluRs. In ACC neurons of adult mice overexpressing dominant active CREB mutant, the upregulation of FMRP by stimulating Group I mGluR is enhanced compared to wild-type mice. However, the regulation of FMRP by Group I mGluRs is not altered by overexpression of Ca2+-insensitive mutant form of downstream regulatory element antagonist modulator (DREAM), a transcriptional repressor involved in synaptic transmission and plasticity. Our study has provided further evidence for CREB involvement in regulation of FMRP by Group I mGluRs in ACC neurons, and may help to elucidate the pathogenesis of fragile X syndrome.
    Molecular Brain 08/2012; 5:27. · 4.20 Impact Factor
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    ABSTRACT: Retinoid signaling pathways mediated by retinoic acid receptor (RAR)/retinoid × receptor (RXR)-mediated transcription play critical roles in hippocampal synaptic plasticity. Furthermore, recent studies have shown that treatment with retinoic acid alleviates age-related deficits in hippocampal long-term potentiation (LTP) and memory performance and, furthermore, memory deficits in a transgenic mouse model of Alzheimer's disease. However, the roles of the RAR/RXR signaling pathway in learning and memory at the behavioral level have still not been well characterized in the adult brain. We here show essential roles for RAR/RXR in hippocampus-dependent learning and memory. In the current study, we generated transgenic mice in which the expression of dominant-negative RAR (dnRAR) could be induced in the mature brain using a tetracycline-dependent transcription factor and examined the effects of RAR/RXR loss. The expression of dnRAR in the forebrain down-regulated the expression of RARβ, a target gene of RAR/RXR, indicating that dnRAR mice exhibit dysfunction of the RAR/RXR signaling pathway. Similar with previous findings, dnRAR mice displayed impaired LTP and AMPA-mediated synaptic transmission in the hippocampus. More importantly, these mutant mice displayed impaired hippocampus-dependent social recognition and spatial memory. However, these deficits of LTP and memory performance were rescued by stronger conditioning stimulation and spaced training, respectively. Finally, we found that pharmacological blockade of RARα in the hippocampus impairs social recognition memory. From these observations, we concluded that the RAR/RXR signaling pathway greatly contributes to learning and memory, and LTP in the hippocampus in the adult brain.
    Molecular Brain 02/2012; 5:8. · 4.20 Impact Factor
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    ABSTRACT: During permanent memory formation, recall of acquired place memories initially depends on the hippocampus and eventually become hippocampus-independent with time. It has been suggested that the quality of original place memories also transforms from a precise form to a less precise form with similar time course. The question arises of whether the quality of original place memories is determined by brain regions on which the memory depends. To directly test this idea, we introduced a new procedure: a non-associative place recognition memory test in mice. Combined with genetic and pharmacological approaches, our analyses revealed that place memory is precisely maintained for 28 days, although the recall of place memory shifts from hippocampus-dependent to hippocampus-independent with time. Moreover, the inactivation of the hippocampal function does not inhibit the precision of remote place memory. These results indicate that the quality of place memories is not determined by brain regions on which the memory depends.
    Molecular Brain 02/2012; 5:5. · 4.20 Impact Factor
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    Yue Zhang, Hotaka Fukushima, Satoshi Kida
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    ABSTRACT: Memory 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. To 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. Our 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.
    Molecular Brain 09/2011; 4:4. · 4.20 Impact Factor
  • Neuroscience Research 09/2011; 71. · 2.20 Impact Factor
  • Neuroscience Research 09/2011; 71. · 2.20 Impact Factor
  • Neuroscience Research 09/2011; 71. · 2.20 Impact Factor
  • Neuroscience Research 09/2011; 71. · 2.20 Impact Factor
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    ABSTRACT: Unraveling the mechanisms by which the molecular manipulation of genes of interest enhances cognitive function is important to establish genetic therapies for cognitive disorders. Although CREB is thought to positively regulate formation of long-term memory (LTM), gain-of-function effects of CREB remain poorly understood, especially at the behavioral level. To address this, we generated four lines of transgenic mice expressing dominant active CREB mutants (CREB-Y134F or CREB-DIEDML) in the forebrain that exhibited moderate upregulation of CREB activity. These transgenic lines improved not only LTM but also long-lasting long-term potentiation in the CA1 area in the hippocampus. However, we also observed enhanced short-term memory (STM) in contextual fear-conditioning and social recognition tasks. Enhanced LTM and STM could be dissociated behaviorally in these four lines of transgenic mice, suggesting that the underlying mechanism for enhanced STM and LTM are distinct. LTM enhancement seems to be attributable to the improvement of memory consolidation by the upregulation of CREB transcriptional activity, whereas higher basal levels of BDNF, a CREB target gene, predicted enhanced shorter-term memory. The importance of BDNF in STM was verified by microinfusing BDNF or BDNF inhibitors into the hippocampus of wild-type or transgenic mice. Additionally, increasing BDNF further enhanced LTM in one of the lines of transgenic mice that displayed a normal BDNF level but enhanced LTM, suggesting that upregulation of BDNF and CREB activity cooperatively enhances LTM formation. Our findings suggest that CREB positively regulates memory consolidation and affects memory performance by regulating BDNF expression.
    Journal of Neuroscience 06/2011; 31(24):8786-802. · 6.91 Impact Factor
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    ABSTRACT: Triggering receptor expressed on myeloid cells (TREM)-1 is expressed in macrophages, and functions as an amplifying molecule in inflammatory responses. TREM-1 is constitutively expressed in macrophage, and upregulated by bacterial components, such as lipopolysaccharide (LPS). In this present study, we investigated the regulatory mechanism for the basal and LPS-induced transcription of mouse TREM-1 gene in mononuclear cells using RAW264.7 macrophage-like cells. To elucidate the potential role of cis-acting elements in the basal and LPS-induced transcription of mouse TREM-1 gene, the luciferase vector containing the promoter with 5' deletion and adenine substitution mutants was transfected into RAW264.7 cells and incubated in the absence or presence of LPS. To further identify the transcription factor(s), gel shift/supershift analysis was performed. The CRE (cAMP response element) and NF-κB-1 (a distal NF-κB site) in the mouse TREM-1 promoter are positively and negatively regulating the basal TREM-1 transcription via the interaction with C/EBPα and NF-κB p50/p50 homodimer, respectively. In addition, the CRE and NF-κB-1 likely participate in the LPS-induced upregulation of TREM-1 promoter activity possibly via the interaction with phosphorylated CREB and NF-κB p65/p50 heterodimer. Furthermore, the AP-1-1 (a distal AP-1 site) is likely to be involved in the LPS-induced TREM-1 transcription via the interaction with phosphorylated c-fos/c-jun. The present study has demonstrated for the first time the detailed mechanism for the basal and LPS-induced expression of TREM-1, an amplifying molecule in inflammation.
    Life sciences 06/2011; 89(3-4):115-22. · 2.56 Impact Factor
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    Ryang Kim, Ryouichi Moki, Satoshi Kida
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    ABSTRACT: Memory retrieval is not a passive process. Recent studies have shown that reactivated memory is destabilized and then restabilized through gene expression-dependent reconsolidation. Molecular studies on the regulation of memory stability after retrieval have focused almost exclusively on fear memory, especially on the restabilization process of the reactivated fear memory. We previously showed that, similarly with fear memories, reactivated spatial memory undergoes reconsolidation in the Morris water maze. However, the underlying molecular mechanisms by which reactivated spatial memory is destabilized and restabilized remain poorly understood. In this study, we investigated the molecular mechanism that regulates the stability of the reactivated spatial memory. We first showed that pharmacological inactivation of the N-methyl-D-aspartate glutamate receptor (NMDAR) in the hippocampus or genetic inhibition of cAMP-responsible element binding protein (CREB)-mediated transcription disrupted reactivated spatial memory. Finally, we showed that pharmacological inhibition of cannabinoid receptor 1 (CB1) and L-type voltage gated calcium channels (LVGCCs) in the hippocampus blocked the disruption of the reactivated spatial memory by the inhibition of protein synthesis. Our findings indicated that the reactivated spatial memory is destabilized through the activation of CB1 and LVGCCs and then restabilized through the activation of NMDAR- and CREB-mediated transcription. We also suggest that the reactivated spatial memory undergoes destabilization and restabilization in the hippocampus, through similar molecular processes as those for reactivated contextual fear memories, which require CB1 and LVGCCs for destabilization and NMDAR and CREB for restabilization.
    Molecular Brain 02/2011; 4:9. · 4.20 Impact Factor
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    ABSTRACT: The teteracycline (Tc)-dependent and -inducible transcriptional activator (rtTA) system has been used to express regulated transgene expression in vitro and in vivo. However, previous reports have demonstrated that, even in the absence of Tc, the rtTA binds weakly to the tetracycline response element (TRE), leading to a low level of background activity. In order to reduce the leaky gene expression induced by rtTA, we previously established a tightly regulated system (A-IRES-R system) that makes use of both the rtTA (A) and a Tc-dependent repressor (TetR-Kruppel-associated box; KRAB) (R). In addition, others have described a transactivator rtTA2-M2 (M2) that displays higher sensitivity to Dox than rtTA. In this study, to further develop the A-IRES-R system, we generated a derivative Tc system (M2-IRES-R system) that co-expresses both rtTA-M2 and TetR-KRAB from a single vector. We show that compared to the A-IRES-R system, the M2-IRES-R system leads to a greater level of induced TRE-mediated transcription in the presence of doxycycline (Dox) and yet displays a similar level of basal TRE-mediated transcription in the absence of Dox. Furthermore, the M2-IRES-R system also displays less leaky gene expression in the absence of Dox compared to rtTA-M2 and rtTA systems. Taken together, our results suggest that the M2-IRES-R system enables to tightly regulate and highly induce the expression of transgene compared to other systems.
    Cytotechnology 02/2011; 63(3):211-6. · 1.32 Impact Factor
  • Satoshi Kida, Hotaka Fukushima, Yue Zhang
    Neuroscience Research - NEUROSCI RES. 01/2011; 71.

Publication Stats

2k Citations
235.03 Total Impact Points

Institutions

  • 2001–2014
    • Tokyo University of Agriculture
      • • Department of Bioscience
      • • Department of Agricultural Chemistry
      • • Faculty of Applied Bioscience
      Edo, Tōkyō, Japan
  • 2012
    • University of Toyama
      • Department of Biochemistry
      Тояма, Toyama, Japan
  • 2008–2012
    • University of Toronto
      • Department of Physiology
      Toronto, Ontario, Canada
  • 2008–2009
    • National Center of Neurology and Psychiatry
      • Department of Ultrastructural Research
      Кодаиры, Tōkyō, Japan
  • 2006
    • University of Pittsburgh
      • Department of Neurobiology
      Pittsburgh, PA, United States
    • SickKids
      • Program in Neurosciences and Mental Health (NMH)
      Toronto, Ontario, Canada
  • 1998
    • Cold Spring Harbor Laboratory
      Cold Spring Harbor, New York, United States