Predominant expression of nuclear activator protein-1 complex with DNA binding activity following systemic administration of N-methyl-d-aspartate in dentate granule cells of murine hippocampus

Yoneda, Yukio; Ogita, Kiyokazu; Azuma, Yasutaka; Kuramoto, Nobuyuki; Manabe, Takayuki; Kitayama, Tomoya

doi:10.1016/s0306-4522(99)00117-7

Cited by 45 publications

(38 citation statements)

References 32 publications

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“…The fact that brief exposure to NMDA induces marked expression of c-Fos, Fos-B, Fra-2, and c-Jun proteins in a manner sensitive to MK-801 (30) is also favorable for the high functionality of NMDAR subunits expressed by neural progenitor cells before differentiation. Rapid responsiveness of AP1 member proteins (30,58) supports the speculation that brief exposure to NMDA could induce transient expression of the AP1 complex via functional NMDAR channels assembled by heteromeric subunits expressed by neural progenitor cells, toward the modulation of de novo synthesis of inducible target proteins responsible for the regulation of cellular proliferation, commitment, differentiation, and/or maturation. Activation of NMDAR would play a key role in the mechanisms associated with commitment and differentiation of neural progenitor cells at an early developmental stage in neurogenesis.…”

Section: A Role Of Nmdar In Neurogenesismentioning

confidence: 75%

“…In our previous studies, an intraperitoneal injection of NMDA led to marked decreases in the incorporation of BrdU and the expression of both nestin and PCNA (24), in addition to the predominant induction of AP1 (23), in the DG of adult mice. These alterations are all antagonized by the prior administration of MK-801 (29,58). Thus, one possible but hitherto unidentified speculation is that WIRS would facilitate the release of glutamate to activate NMDAR toward subsequent suppression of the proliferation of neural progenitor cells in the DG.…”

Section: Adult Neurogenesismentioning

confidence: 99%

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Neurogenesis Mediated by γ-Aminobutyric Acid and Glutamate Signaling

2009

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Abstract. In this review, we will summarize our ongoing studies on the functionality of both γ-aminobutyric acid (GABA) and glutamate receptors expressed by undifferentiated neural progenitor cells isolated from embryonic rodent brains. Cells were cultured with growth factors for the formation of round spheres by clustered cells under floating conditions, whereas a reverse transcription polymerase chain reaction analysis revealed expression of mRNA for particular subtypes of different ionotropic and metabotropic GABA and glutamate receptors in undifferentiated progenitors and neurospheres. Moreover, sustained exposure to either GABAergic or glutamatergic agonists not only modulated the size of neurospheres formed, but also affected spontaneous and induced differentiation of neural progenitor cells into particular progeny cell lineages such as neurons and astroglia. Both GABA and glutamate could play a pivotal role in the mechanisms underlying proliferation for self-replication along with the determination of subsequent differentiation fate toward particular progeny lineages through activation of their receptor subtypes functionally expressed by undifferentiated neural progenitor cells. Accordingly, neurogenesis seems to be also under control by GABAergic and glutamatergic signaling in developing brains as seen with neurotransmission in adult brains.

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Section: A Role Of Nmdar In Neurogenesismentioning

confidence: 75%

Section: Adult Neurogenesismentioning

confidence: 99%

Neurogenesis Mediated by γ-Aminobutyric Acid and Glutamate Signaling

2009

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“…[39][40][41] min at 251C with 10 mg RNase A, followed by the addition of a four-fold volume of SDS-PAGE sample dye mixture [10 mM Tris-HCl (pH 6.8), 10% glycerol, 2% sodium dodecyl sulfate (SDS), 0.01% bromophenol blue, and 5% 2-mercaptoethanol]. This sample mixture was separated by SDS-PAGE (15 or 10-20% gradient of polyacrylamide).…”

Section: Preparation Of Nuclear Extracts Cytosolic Fractions and Nucmentioning

confidence: 99%

Induced HMGA1a expression causes aberrant splicing of Presenilin-2 pre-mRNA in sporadic Alzheimer's disease

et al. 2003

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The aberrant splicing isoform (PS2V), generated by exon 5 skipping of the Presenilin-2 (PS2) gene transcript, is a diagnostic feature of sporadic Alzheimer's disease (AD). We found PS2V is hypoxia-inducible in human neuroblastoma SK-N-SH cells. We purified a responsible trans-acting factor based on its binding to an exon 5 fragment. The factor was identified as the high mobility group A1a protein (HMGA1a; formerly HMG-I). HMGA1a bound to a specific sequence on exon 5, located upstream of the 5 0 splice site. HMGA1a expression was induced by hypoxia and the protein was accumulated in the nuclear speckles with the endogenous splicing factor SC35. Overexpression of HMGA1a generated PS2V, but PS2V was repressed by cotransfection with the U1 snRNP 70K protein that has a strong affinity to HMGA1a. HMGA1a could interfere with U1 snRNP binding to the 5 0 splice site and caused exon 5 skipping. HMGA1a levels were significantly increased in the brain tissue from sporadic AD patients. We propose a novel mechanism of sporadic AD that involves HMGA1a-induced aberrant splicing of PS2 premRNA in the absence of any mutations.

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“…In vivo administration of NMDA leads to expression of c-Fos protein and potentiation of AP1 DNA binding in murine brain (11), while the potentiation of AP1 DNA binding is highly selective for the hippocampus among the discrete brain structures (12). In murine hippocampus, the systemic administration of NMDA results in preferential potentiation of AP1 DNA binding in the dentate granule cells, but not in the CA1 and CA3 pyramidal layers (13). In addition to the nuclear extracts described above, NMDA is also effective in potentiating AP1 DNA binding constitutively detected in cytosolic fractions of murine hippocampus (14).…”

Section: Glutamatementioning

confidence: 99%

Transcription Factors and Drugs in the Brain

Nakamichi

Yoneda

2002

Japanese Journal of Pharmacology

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ABSTRACT-In mammalian cells, protein de novo synthesis is mainly regulated at the stage of gene transcription by RNA polymerase II in the nucleus. Transcription factors are proteins that bind to the specific nucleotide sequences at promoter or enhancer regions on target genes to control the transcription of mRNA from genomic DNA. In this article, we have outlined the signal responsiveness of different transcription factors to particular drugs in the brain. Nuclear transcription factors rapidly respond to a variety of extracellular signals carried by neurotransmitters, hormones and autacoids as a third messenger in frequent situations. Translated proteins are responsible for a number of physiological and pathological events for a long period in the brain. We have also discussed possible involvement of transcription factors in molecular mechanisms underlying development of tolerance and dependence to drugs following acute and chronic administration.

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Predominant expression of nuclear activator protein-1 complex with DNA binding activity following systemic administration of N-methyl-d-aspartate in dentate granule cells of murine hippocampus

Cited by 45 publications

References 32 publications

Neurogenesis Mediated by γ-Aminobutyric Acid and Glutamate Signaling

Neurogenesis Mediated by γ-Aminobutyric Acid and Glutamate Signaling

Induced HMGA1a expression causes aberrant splicing of Presenilin-2 pre-mRNA in sporadic Alzheimer's disease

Transcription Factors and Drugs in the Brain

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