Postnatal Touch Stimulation Acutely Alters Corticosterone Levels and Glucocorticoid Receptor Gene Expression in the Neonatal Rat

Jutapakdeegul, Nuanchan; Casalotti, Stefano O.; Govitrapong, Piyarat; Kotchabhakdi, Naiphinich

doi:10.1159/000071465

Cited by 68 publications

(60 citation statements)

References 33 publications

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“…Moreover, artificial tactile stimulation derived from simply stroking the pups with a brush is sufficient to increase NGFI-A association with the exon 1 7 promoter. These findings are consistent with an earlier report showing that the same 'stroking' of pups increases hippocampal GR expression [38] and dampens HPA responses to stress [39]. These findings suggest that it is the tactile stimulation associated with pup LG that is critical for the effect on hippocampal NGFI-A association with the exon 1 7 GR promoter.…”

Section: How Do Parental Signals Alter Dna Methylation?supporting

confidence: 92%

Environmental regulation of the neural epigenome

et al. 2011

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a b s t r a c tParental effects are a major source of phenotypic plasticity. Moreover, there is evidence from studies with a wide range of species that the relevant parental signals are influenced by the quality of the parental environment. The link between the quality of the environment and the nature of the parental signal is consistent with the idea that parental effects, whether direct or indirect, might serve to influence the phenotype of the offspring in a manner that is consistent with the prevailing environmental demands. In this review we explore recent studies from the field of 'environmental epigenetics' that suggest that (1) DNA methylation states are far more variable than once thought and that, at least within specific regions of the genome, there is evidence for both demethylation and remethylation in post-mitotic cells and (2) that such remodeling of DNA methylation can occur in response to environmentally-driven, intracellular signaling pathways. Thus, studies of variation in mother-offspring interactions in rodents suggest that parental signals operate during pre-and/ or post-natal life to influence the DNA methylation state at specific regions of the genome leading to sustained changes in gene expression and function. We suggest that DNA methylation is a candidate mechanism for parental effects on phenotypic variation.

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Section: How Do Parental Signals Alter Dna Methylation?supporting

confidence: 92%

Environmental regulation of the neural epigenome

et al. 2011

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“…Jutapakdeegul et al (2003) report that enhanced tactile stimulation (pup stroking with a brush) over the first week of life results in increased hippocampal GR expression in adulthood. Previous studies suggest that such effects as well as those on NGFI-A expression are mediated by increased hippocampal 5-HT activity at 5-HT 7 receptors that are positively coupled to cAMP (Mitchell et al, 1990(Mitchell et al, , 1992Meaney et al, 2000).…”

mentioning

confidence: 96%

The Transcription Factor Nerve Growth Factor-Inducible Protein A Mediates Epigenetic Programming: Altering Epigenetic Marks by Immediate-Early Genes

Weaver¹,

D’Alessio²,

Brown³

et al. 2007

J. Neurosci.

469

422

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Maternal care alters epigenetic programming of glucocorticoid receptor (GR) gene expression in the hippocampus, and increased postnatal maternal licking/grooming (LG) behavior enhances nerve growth factor-inducible protein A (NGFI-A) transcription factor binding to the exon 1 7 GR promoter within the hippocampus of the offspring. We tested the hypothesis that NGFI-A binding to the exon 1 7 GR promoter sequence marks this sequence for histone acetylation and DNA demethylation and that such epigenetic alterations subsequently influence NGFI-A binding and GR transcription. We report that (1) NGFI-A binding to its consensus sequence is inhibited by DNA methylation, (2) NGFI-A induces the activity of exon 1 7 GR promoter in a transient reporter assay, (3) DNA methylation inhibits exon 1 7 GR promoter activity, and (4) whereas NGFI-A interaction with the methylated exon 1 7 GR promoter is reduced, NGFI-A overexpression induces histone acetylation, DNA demethylation, and activation of the exon 1 7 GR promoter in transient transfection assays. Site-directed mutagenesis assays demonstrate that NGFI-A binding to the exon 1 7 GR promoter is required for such epigenetic reprogramming. In vivo, enhanced maternal LG is associated with increased NGFI-A binding to the exon 1 7 GR promoter in the hippocampus of pups, and NGFI-A-bound exon 1 7 GR promoter is unmethylated compared with unbound exon 1 7 GR promoter. Knockdown experiments of NGFI-A in hippocampal primary cell culture show that NGFI-A is required for serotonin-induced DNA demethylation and increased exon 1 7 GR promoter expression. The data are consistent with the hypothesis that NGFI-A participates in epigenetic programming of GR expression.

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“…The Reverse transcriptase polymerase chain reaction (RT-PCR) was carried out using the Qiagen one step RT-PCR kit. PCR amplifications of SAT1 employed primers 5 -ACAGGC-GACATTCTCATCCT-3 (forward) and 5 -GTTTCA-GTGGCCTTCACCAT-3 (reverse), giving rise to a 426 base pair amplicon 24 , and β-actin (housekeeping gene) primers 5 -CCCAGAGCAAGAGAGGCATC-3 (forward) and 5 -CTCAGGAGGAGCAATGATCT-3 (reverse), giving rise to a 830 base pair amplicon 25 . Primers were obtained from the Bioservice Unit of the National Science and Technology Development Agency, Thailand.…”

Section: Methodsmentioning

confidence: 99%

“…Recently, our group demonstrated that treatment of mixed cell cultures with 10 µM Aβ (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35) for 12 h and 24 h reduces SAT1 protein level as demonstrated by immunocytochemical and quantitative immunoreactivity analysis 20 . We now report the effects of Aβ(25-35) on SAT1 expression in rat cortical primary cell cultures.…”

Section: Introductionmentioning

confidence: 98%

“…A small 11-amino acid fragment of the fulllength peptide, Aβ (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35), is a convenient alternative in Alzheimer's disease investigations as the peptide mimics several toxicological and oxidative stress properties of the native full-length peptide 4,18,19 . Recently, our group demonstrated that treatment of mixed cell cultures with 10 µM Aβ (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35) for 12 h and 24 h reduces SAT1 protein level as demonstrated by immunocytochemical and quantitative immunoreactivity analysis 20 .…”

Section: Introductionmentioning

confidence: 99%

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Buntup¹,

Chayasadom²,

Surarit³

et al. 2009

ScienceAsia

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ABSTRACT:Alzheimer's disease is a major neurodegenerative disorder in which there is an overproduction and accumulation of amyloid-β (Aβ) peptides. During the initial stages of the disease, glutamate receptors are dysregulated by Aβ accumulation resulting in the disruption of glutamatergic synaptic transmission. We used rat cortical cell cultures to examine the effects of Aβ(25-35)-induced neurotoxicity on glutamine transporters involved in the glutamate cycle. In primary mixed cell cultures prepared from cerebral cortex, incubation with 10 µM Aβ(25-35) for 12 h, but not for 24 h, markedly suppressed system A transporter 1 (SAT1) mRNA expression. On the other hand, Aβ(25-35) had no effect on SAT1 mRNA level in neuronal cell cultures. Treatment of both types of cell cultures with Aβ(25-35) resulted in a significant decrease in cell survival in a concentration and time-dependent manner, as determined by MTT assay. These results indicated that Aβ may impair neuronal function and transmitter synthesis and perhaps reduce excitotoxicity through a reduction in neuronal glutamine uptake.

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Postnatal Touch Stimulation Acutely Alters Corticosterone Levels and Glucocorticoid Receptor Gene Expression in the Neonatal Rat

Cited by 68 publications

References 33 publications

Environmental regulation of the neural epigenome

Environmental regulation of the neural epigenome

The Transcription Factor Nerve Growth Factor-Inducible Protein A Mediates Epigenetic Programming: Altering Epigenetic Marks by Immediate-Early Genes

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