mRNA distribution in adult human brain of GRIN2B, a N-methyl-d-aspartate (NMDA) receptor subunit

Schito, Anna Maria; Pizzuti, Antonio; Maria, Emilio Di; Schenone, Aldo L.; Ratti, Angelo; Defferrari, Raffaella; Bellone, Emilia; Mancardi, Gianluigi; Ajmar, Franco; Mandich, Paola

doi:10.1016/s0304-3940(97)00853-7

Cited by 42 publications

(31 citation statements)

References 21 publications

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“…The GRIN2B gene is mainly expressed in forebrain structures such as the hippocampus, striatum, thalamus and olfactory bulb [17]. Its altered expression at the protein level has been observed in bipolar disorder [16]; however, it was not confirmed by a recent study by Martucci et al [9].…”

Section: Introductionmentioning

confidence: 94%

No association of three GRIN2B polymorphisms with lithium response in bipolar patients

Szczepankiewicz

Skibińska

Suwalska

et al. 2009

Pharmacological Reports

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Abstract:We investigated three polymorphisms in the NMDA receptor 2B subunit gene (GRIN2B) as a candidate gene for lithium response involved in glutamatergic neurotransmission. One hundred five bipolar patients treated with lithium for at least 5 years were analyzed. The lithium response was assessed as excellent -no affective episodes during lithium treatment; partial -50% reduction in the episode index; or no response -less than 50% reduction, no change or worsening in the episode index. Genotypes for the -200G/T, 366C/G and rs890G/T GRIN2B polymorphisms were established using the PCR-RFLP method. Genotype distributions were in Hardy-Weinberg equilibrium for all three polymorphisms. No association was found between the three polymorphisms studied and the treatment response to lithium. The authors conclude that polymorphisms of the GRIN2B gene did not show an association with the treatment response to lithium in bipolar patients.

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Section: Introductionmentioning

confidence: 94%

No association of three GRIN2B polymorphisms with lithium response in bipolar patients

Szczepankiewicz

Skibińska

Suwalska

et al. 2009

Pharmacological Reports

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“…Generally, NMDARs are found in a heteromeric state composed of two copies each of the glycine binding GluN1 subunits, glutamate binding-GluN2 subunit and/or GluN3 subunits (Furukawa et al 2005;Flores-Soto et al 2012). In the LA, NMDARs are largely composed of either the GluN2A or GluN2B subunit in addition to the GluN1 subunit (Schito et al 1997) and it has been shown that the GluN2B subunit is critical for fear learning, whereas the GluN2A subunit has stronger implications in fear expression (Rodrigues et al 2001). Indeed, overexpression of the GluN2B subunit in genetically modified mice revealed enhanced fear-conditioned performance relative to wild-type controls (Tang et al 1999).…”

Section: Histone H3 Lysine Methylation In the Lamentioning

confidence: 99%

NMDA receptor- and ERK-dependent histone methylation changes in the lateral amygdala bidirectionally regulate fear memory formation

et al. 2014

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It is well established that fear memory formation requires de novo gene transcription in the amygdala. We provide evidence that epigenetic mechanisms in the form of histone lysine methylation in the lateral amygdala (LA) are regulated by NMDA receptor (NMDAR) signaling and involved in gene transcription changes necessary for fear memory consolidation. Here we found increases in histone H3 lysine 9 dimethylation (H3K9me2) levels in the LA at 1 h following auditory fear conditioning, which continued to be temporally regulated up to 25 h following behavioral training. Additionally, we demonstrate that inhibiting the H3K9me2 histone lysine methyltransferase G9a (H/KMTs-G9a) in the LA impaired fear memory, while blocking the H3K9me2 histone lysine demethylase LSD1 (H/KDM-LSD1) enhanced fear memory, suggesting that H3K9me2 in the LA can bidirectionally regulate fear memory formation. Furthermore, we show that NMDAR activity differentially regulated the recruitment of H/KMT-G9a, H/KDM-LSD1, and subsequent H3K9me2 levels at a target gene promoter. This was largely regulated by GluN2B-but not GluN2A-containing NMDARs via ERK activation. Moreover, fear memory deficits associated with NMDAR or ERK blockade were successfully rescued through pharmacologically inhibiting LSD1, suggesting that enhancements of H3K9me2 levels within the LA can rescue fear memory impairments that result from hypofunctioning NMDARs or loss of ERK signaling. Together, the present study suggests that histone lysine methylation regulation in the LA via NMDAR-ERK-dependent signaling is involved in fear memory formation.

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“…It is expressed in the hippocampus, basal ganglia, and cerebral cortex. 7 The GRIN1 gene has been found to be underexpressed in the cortex of schizophrenics 8 and has been suggested as a likely candidate in the pharmacogenetics of typical and atypical antipsychotics. 9 Evidence of studies on functional expression 10,11 and a mouse model 12 support the GRIN2B gene as a candidate for schizophrenia.…”

Section: Gene Variantsmentioning

confidence: 99%

Association study between the NMDA receptor 2B subunit gene (GRIN2B) and schizophrenia: A HuGE review and meta-analysis

2007

Genetics in Medicine

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mRNA distribution in adult human brain of GRIN2B, a N-methyl-d-aspartate (NMDA) receptor subunit

Cited by 42 publications

References 21 publications

No association of three GRIN2B polymorphisms with lithium response in bipolar patients

No association of three GRIN2B polymorphisms with lithium response in bipolar patients

NMDA receptor- and ERK-dependent histone methylation changes in the lateral amygdala bidirectionally regulate fear memory formation

Association study between the NMDA receptor 2B subunit gene (GRIN2B) and schizophrenia: A HuGE review and meta-analysis

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