Neuromodulatory Effect of Gαs- or Gαq-Coupled G-Protein-Coupled Receptor on NMDA Receptor Selectively Activates the NMDA Receptor/Ca2+/Calcineurin/cAMP Response Element-Binding Protein-Regulated Transcriptional Coactivator 1 Pathway to Effectively Induce Brain-Derived Neurotrophic Factor Expression in Neurons

Fukuchi, Mamoru; Tabuchi, Akiko; Kuwana, Yuki; Watanabe, Shinjiro; Inoue, Motomichi; Takasaki, Ichiro; Izumi, Hironori; Tanaka, Ayumi; Inoue, Ran; Mori, Hisashi; Komatsu, Hidetoshi; Takemori, Hiroshi; Okuno, Hiroyuki; Bito, Haruhiko; Tsuda, Masashi

doi:10.1523/jneurosci.3650-14.2015

Cited by 58 publications

(84 citation statements)

References 69 publications

(18 reference statements)

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“…Furthermore, a connection between CaN and NMDARs has been presented. For example, CaN pathway that is controlled by calcium signals evoked via NMDARs mediates NMDAR activation-induced BDNF expression [61]; CaN inhibitor FK506 upregulates NR2C expression in CGNs [62], suggesting a negative regulation of NR2C by CaN. Collectively, we propose that CaN may be an inhibitory mediator that conveys JAK/STAT3 signaling to NMDAR subunits to inhibit their activities in IL-6 neuroprotection.…”

Section: Discussionmentioning

confidence: 79%

Interleukin-6 reduces NMDAR-mediated cytosolic Ca2+ overload and neuronal death via JAK/CaN signaling

Zhuang

Shen

et al. 2015

Cell Calcium

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Section: Discussionmentioning

confidence: 79%

Interleukin-6 reduces NMDAR-mediated cytosolic Ca2+ overload and neuronal death via JAK/CaN signaling

Zhuang

Shen

et al. 2015

Cell Calcium

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“…In the case of primary culture mRNA detection, the preparation of cultured rat primary neuron, cultured mice astrocyte and cultured microglia were described as previous methods 51–53 . Total RNA (500 ng) from each cells sample was transcribed into the cDNA and then the quantitative real time RT-PCR was run following the manufacturer’s instructions.…”

Section: Methodsmentioning

confidence: 99%

Involvement of the accumbal osteopontin-interacting transmembrane protein 168 in methamphetamine-induced place preference and hyperlocomotion in mice

Miyamoto

Otake

et al. 2017

Sci Rep

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Chronic exposure to methamphetamine causes adaptive changes in brain, which underlie dependence symptoms. We have found that the transmembrane protein 168 (TMEM168) is overexpressed in the nucleus accumbens of mice upon repeated methamphetamine administration. Here, we firstly demonstrate the inhibitory effect of TMEM168 on methamphetamine-induced behavioral changes in mice, and attempt to elucidate the mechanism of this inhibition. We overexpressed TMEM168 in the nucleus accumbens of mice by using an adeno-associated virus vector (NAc-TMEM mice). Methamphetamine-induced hyperlocomotion and conditioned place preference were attenuated in NAc-TMEM mice. Additionally, methamphetamine-induced extracellular dopamine elevation was suppressed in the nucleus accumbens of NAc-TMEM mice. Next, we identified extracellular matrix protein osteopontin as an interacting partner of TMEM168, by conducting immunoprecipitation in cultured COS-7 cells. TMEM168 overexpression in COS-7 cells induced the enhancement of extracellular and intracellular osteopontin. Similarly, osteopontin enhancement was also observed in the nucleus accumbens of NAc-TMEM mice, in in vivo studies. Furthermore, the infusion of osteopontin proteins into the nucleus accumbens of mice was found to inhibit methamphetamine-induced hyperlocomotion and conditioned place preference. Our studies suggest that the TMEM168-regulated osteopontin system is a novel target pathway for the therapy of methamphetamine dependence, via regulating the dopaminergic function in the nucleus accumbens.

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“…In the nucleus, CRTC1 increases the expression of a subset of CREB target genes, including c-fos, Arc, Nr4a1, Bdnf (Ch'ng et al, 2012; Fukuchi et al, 2015; Nonaka et al, 2014; Parra-Damas et al, 2017; Parra-Damas et al, 2014; Zhou et al, 2006a) (Fig. 1).…”

Section: Crtc1-creb Signaling In Memory Enhancementmentioning

confidence: 99%

Epigenetic regulation of Fgf1 transcription by CRTC1 and memory enhancement

Uchida

Shumyatsky

2018

Brain Research Bulletin

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Recent evidence demonstrates that epigenetic regulation of gene transcription is critically involved in learning and memory. Here, we discuss the role of histone acetylation and DNA methylation, which are two best understood epigenetic processes in memory processes. More specifically, we focus on learning-strength-dependent changes in chromatin on the fibroblast growth factor 1 (Fgf1) gene and on the molecular events that modulate regulation of Fgf1 transcription, required for memory enhancement, with the specific focus on CREB-regulated transcription coactivator 1 (CRTC1).

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Abstract: Although coordinated molecular signaling through excitatory and modulatory neurotransmissions is critical for the induction of immediate early genes (IEGs), which lead to effective changes in synaptic plasticity, the intracellular mechanisms responsible remain obscure.

Cited by 58 publications

References 69 publications

Interleukin-6 reduces NMDAR-mediated cytosolic Ca2+ overload and neuronal death via JAK/CaN signaling

Interleukin-6 reduces NMDAR-mediated cytosolic Ca2+ overload and neuronal death via JAK/CaN signaling

Involvement of the accumbal osteopontin-interacting transmembrane protein 168 in methamphetamine-induced place preference and hyperlocomotion in mice

Epigenetic regulation of Fgf1 transcription by CRTC1 and memory enhancement

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