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bdnf -brain derived neurotrophic factor
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Gene-specific methylation control of H3K9 and H3K36 on neurotrophic BDNF versus astroglial GFAP genes by KDM4A/C regulates neural stem cell differentiation.
Journal: Journal of molecular biology
December/7/2014
Description

Neural stem cell (NSC) state and fate depend on spatially and temporally synchronized transcriptional and epigenetic regulation of the expression of extrinsic signaling factors and intrinsic cell-specific genes, but the functional roles for chromatin-modifying enzymes in neural differentiation remain poorly understood. Here we show that the histone demethylases KDM4A (JMJD2A) and KDM4C (JMJD2C) are essential for proper differentiation of NSCs in vitro and in vivo. KDM4A/C were required for neuronal differentiation, survival and expression of the neurotrophic signaling factor BDNF in association with promoter H3K9 demethylation and RNA polymerase II recruitment. Unexpectedly, KDM4A/C were essential for selective H3K36 demethylation and loss of RNA polymerase II recruitment in transcribed regions of the astrocyte-characteristic gene GFAP, thereby in parallel repressing astrocytic differentiation by control of elongation. We propose that gene- and lysine-specific KDM4A/C-mediated control of histone methylation and thereby regulation of intrinsic factors and signaling factors such as BDNF provide a novel control mechanism of lineage decision.

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Pubmed
Increased serum brain-derived neurotrophic factor protein upon hypoxia in healthy young men.
Journal: Journal of neural transmission (Vienna, Austria : 1996)
January/13/2010
Description

Exposing animals to brief hypoxic periods leads to neuroprotective ischemic tolerance termed preconditioning. This phenomenon is well documented in the brain, but the underlying mechanisms require further elucidation. As nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) are important mediators of maintaining homeostatic conditions in the adult nervous system in terms of physiological and pathophysiological processes, we hypothesized that hypoxic preconditioning might modulate serum neurotrophin concentrations. Hypoxia was induced for 30 min in 14 healthy young men resulting in a constant blood oxygen saturation of 75%. Hyperinsulinemic euglycemic clamps were performed and serum concentrations of BDNF and NGF were measured at baseline, directly after the intervention, and at the end of the session. Overall, serum BDNF concentrations decreased over time by maximally 35% (P = 0.001) while in contrast NGF concentrations remained unchanged. Acute hypoxia alleviated the decrease of BDNF resulting in higher BDNF concentrations as compared to normoxic control (P < 0.01). Our findings show that acute hypoxia results in significantly higher serum BDNF concentrations pointing to a potential role of BDNF in the underlying mechanism of hypoxic preconditioning. Based on its neuroprotective properties, BDNF may be of high clinical relevance for therapeutic options in ischemic neurovascular diseases.

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Pubmed
COMT Val(158)Met and BDNF C(270)T polymorphisms in schizophrenia: a case-control study.
Journal: Schizophrenia research
May/9/2005
Description

In a multicenter study involving 217 subjects of European ancestry [106 patients with schizophrenia and 111 healthy subjects], we tested the hypothesis that the catechol-O-methyl transferase (COMT) Val(158)Met and/or the brain-derived neurotrophic factor (BDNF) C(270)T gene polymorphisms are associated with schizophrenia. The COMT and BDNF genotype and their allele distribution did not differ between patients with schizophrenia and healthy comparison subjects. These results do not support the hypothesis that the COMT Val(158)Met or BDNF C(270)T gene polymorphisms are associated with liability to schizophrenia.

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Pubmed
Comparative mapping between humans and pigs: localization of 58 anchorage markers (TOASTs) by use of porcine somatic cell and radiation hybrid panels.
Journal: Mammalian genome : official journal of the International Mammalian Genome Society
February/21/2001
Description

To increase the number of Type I markers that are directly informative for comparative mapping, 58 anchorage markers, TOASTs (Traced Orthologous Amplified Sequence Tags), were mapped in pig. With specific consensus primers, 76 TOASTs were tested in pig: 50 were regionally localized in pig on a somatic cell hybrid panel (SCHP), and 51 were mapped on the whole genome, INRA/University of Minnesota porcine Radiation Hybrid panel (IMpRH). Comparison of marker positions on RH and cytogenetic maps indicated general concordance except for two chromosomal regions. For RH mapping, all markers, apart from one, were significantly linked (LOD > 4.8) to a marker of the first-generation radiation hybrid map. Localization of new markers on the initial map is necessary for drawing a framework map as shown for Chromosome Sscr 14. The addition of four TOASTs has enabled us to propose an improved map, using a threshold likelihood ratio of 1000/1. At the whole-genome level, this work significantly increased (by 50%) the number of precisely mapped genes on the porcine RH map and confirmed that the IMpRH panel is a valuable tool for high-resolution gene mapping in pig. Porcine PCR products were sequenced and compared with human sequences to verify their identity. Most of the localizations made it possible to either confirm or refine the previous comparative data between humans and pigs obtained through heterologous chromosomal painting or gene mapping. Moreover, the use of TOASTs in mapping studies appears to be a complement to other strategies using CATS, human ESTs, or heterologous FISH with BACs which had already been applied to improve the gene density of comparative genomic maps for mammals.

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Pubmed
Early exposure to ethanol or red wine and long-lasting effects in aged mice. A study on nerve growth factor, brain-derived neurotrophic factor, hepatocyte growth factor, and vascular endothelial growth factor.
Journal: Neurobiology of aging
April/18/2012
Description

Prenatal ethanol exposure produces severe changes in brain, liver, and kidney through mechanisms involving growth factors. These molecules regulate survival, differentiation, maintenance, and connectivity of brain, liver, and kidney cells. Despite the abundant available data on the short and mid-lasting effects of ethanol intoxication, only few data show the long-lasting damage induced by early ethanol administration. The aim of this study was to investigate changes in nerve growth factor (NGF), brain derived neurotrophic factor (BDNF), hepatocyte growth factor (HGF), and vascular endothelial growth factor (VEGF) in brain areas, liver, and kidney of 18-mo-old male mice exposed perinatally to ethanol at 11% vol or to red wine at the same ethanol concentration. The authors found that ethanol per se elevated NGF, BDNF, HGF, and VEGF measured by ELISA in brain limbic system areas. In the liver, early exposure to ethanol solution and red wine depleted BDNF and VEGF concentrations. In the kidney, red wine exposure only decreased VEGF. In conclusion, the present study shows that, in aged mice, early administration of ethanol solution induced long-lasting damage at growth factor levels in frontal cortex, hippocampus, and liver but not in kidney. Otherwise, in mice exposed to red wine, significant changes were observed in the liver and kidney but not in the hippocampus and frontal cortex. The brain differences in ethanol-induced toxicity when ethanol is administered alone or in red wine may be related to compounds with antioxidant properties present in the red wine.

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Pubmed
Working memory task decreases the survival of newly born neurons in hippocampus.
Journal: Neurobiology of learning and memory
August/2/2011
Description

Throughout life new neurons are generated in dentate gyrus of hippocampus. Previous studies have found that spatial tasks can rescue newly born neurons from death. However, it is still unknown whether new neurons are similarly affected by all types of hippocampal-dependent tasks. Here we investigated the possible effects of working memory task (WMT) on immature neurons. Mice were trained in reference memory task and WMT respectively. The reference memory task used the classical hidden platform (HP) water maze task, while WMT used a delayed matching-to-place (DMTP) water maze task. Bromodeoxyuridine (BrdU) was administrated during the early or late phase of training, or 1week prior to training, in order to label dividing proliferating cells. After water maze training, the number of BrdU-labeled cells in dentate gyrus of hippocampus was compared. In addition, hippocampal brain-derived neurotrophic factor (BDNF) and Notch 1 receptor were characterized using Western blot. Serum corticosterone levels were also measured using enzyme immunoassay. Results showed that HP task and DMTP task did not change the number of BrdU-labeled cells produced during the early or late phase of training. As expected, the HP task increased the number of BrdU-labeled cells produced 1 week prior to training. However, DMTP task decreased the number of BrdU-labeled cells produced 1 week prior to training. Both tasks lead to a significant increase in serum corticosterone levels and did not change the expression of BDNF and Notch 1 receptor in hippocampus. Taken together, these results demonstrate that WMT has different effects on survival of immature neurons, and therefore suggests immature neurons may have more than one role depending on the demands of the tasks.

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Pubmed
Association study in eating disorders: TPH2 associates with anorexia nervosa and self-induced vomiting.
Journal: Genes, brain, and behavior
June/14/2011
Description

Twin studies suggest that genetic factors play a substantial role in anorexia nervosa (AN) and self-induced vomiting (SV), a key symptom that is shared among different types of eating disorders (EDs). We investigated the association of 25 single nucleotide polymorphisms (SNPs), capturing 71-91% of the common variance in candidate genes, stathmin (STMN1), serotonin receptor 1D (HTR1D), tryptophan hydroxylase 2 (TPH2) and brain-derived neurotrophic factor (BDNF), with AN and EDs characterized by regular SV. The first allele frequencies of all the SNPs were compared between a Dutch case group (182 AN, 149 EDs characterized by SV) and 607 controls. Associations rendering P-values < 0.05 from this initial study were then tested for replication in a meta-analysis with two additional independent ED case-control samples, together providing 887 AN cases, 306 cases with an ED characterized by SV and 1914 controls. A significant effect for the minor C-allele of tryptophan hydroxylase 2 rs1473473 was observed for both AN [odds ratio (OR) = 1.30, 95% CI 1.08-1.57, P < 0.003] and EDs characterized by SV (OR = 1.52, 95% CI 1.28-2.04, P < 0.006). In the combined case group, a dominant effect was observed for rs1473473 (OR = 1.38, 95% CI 1.16-1.64, P < 0.0003). The meta-analysis revealed that the tryptophan hydroxylase 2 polymorphism rs1473473 was associated with a higher risk for AN, EDs characterized by SV and for the combined group.

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Pubmed
The expression mechanism of the residual LTP in the CA1 region of BDNF k.o. mice is insensitive to NO synthase inhibition.
Journal: Brain research
August/29/2011
Description

BDNF and nitric oxide signaling both contribute to long-term potentiation (LTP) at glutamatergic synapses, but to date, few studies analyzed the interaction of both signaling cascades in the same synaptic pathway. Here we addressed the question whether the residual LTP in the CA1 region of hippocampal slices from heterozygous BDNF knockout mice (BDNF⁺/⁻) is dependent on nitric oxide (NO) signaling. Extracellular recording of synaptic field potentials elicited by presynaptic Schaffer collateral stimulation was performed in the CA1 region of hippocampal slices of 4- to 6-week-old mice, and LTP was induced by a theta burst stimulation protocol. Application of the nitric oxide inhibitor L-NAME (200 μM) strongly inhibited LTP by 70% in wildtype animals. This inhibition of LTP was not a consequence of altered basal synaptic properties. In CA1 of BDNF⁺/⁻ mice, stimulated with the same theta burst protocol, LTP was reduced by 50% as compared to wildtype animals. This impairment in the expression of LTP in BDNF⁺/⁻ mice did not result from an increased synaptic fatigue. The residual LTP in BDNF⁺/⁻ was not further reduced by preincubation of slices with L-NAME. These results suggest that BDNF and NO share overlapping intracellular signaling cascades to mediate LTP in CA1, and part of their signaling cascades are most likely arranged consecutively in the signaling pathway mediating LTP.

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Pubmed
Association analysis of serotonin receptor 1B (HTR1B) and brain-derived neurotrophic factor gene polymorphisms in Borderline personality disorder.
Journal: Journal of neural transmission (Vienna, Austria : 1996)
September/29/2009
Description

The purpose of this study was to test for association between Borderline personality disorder (BPD) and variants of the HTR1B and the brain-derived neurotrophic factor (BDNF) gene. We genotyped four HTR1B and the functional BDNF G196A marker in 161 Caucasian BPD patients and 156 healthy controls. There were no significant differences between groups in genotype or haplotype distribution of HTR1B markers or in genotype distribution of the BDNF marker. Logistic regression analyses revealed an over-representation of the BDNF 196A allele in HTR1B A-161 allele carrying BPD patients.

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Pubmed
Developmental fluoxetine exposure increases behavioral despair and alters epigenetic regulation of the hippocampal BDNF gene in adult female offspring.
Journal: Hormones and behavior
December/12/2016
Description

A growing number of infants are exposed to selective serotonin reuptake inhibitor (SSRI) medications during the perinatal period. Perinatal exposure to SSRI medications alter neuroplasticity and increase depressive- and anxiety-related behaviors, particularly in male offspring as little work has been done in female offspring to date. The long-term effects of SSRI on development can also differ with previous exposure to prenatal stress, a model of maternal depression. Because of the limited work done on the role of developmental SSRI exposure on neurobehavioral outcomes in female offspring, the aim of the present study was to investigate how developmental fluoxetine exposure affects anxiety and depression-like behavior, as well as the regulation of hippocampal brain-derived neurotrophic factor (BDNF) signaling in the hippocampus of adult female offspring. To do this female Sprague-Dawley rat offspring were exposed to prenatal stress and fluoxetine via the dam, for a total of four groups of female offspring: 1) No Stress+Vehicle, 2) No Stress+Fluoxetine, 3) Prenatal Stress+Vehicle, and 4) Prenatal Stress+Fluoxetine. Primary results show that, in adult female offspring, developmental SSRI exposure significantly increases behavioral despair measures on the forced swim test, decreases hippocampal BDNF exon IV mRNA levels, and increases levels of the repressive histone 3 lysine 27 tri-methylated mark at the corresponding promoter. There was also a significant negative correlation between hippocampal BDNF exon IV mRNA levels and immobility in the forced swim test. No effects of prenatal stress or developmental fluoxetine exposure were seen on tests of anxiety-like behavior. This research provides important evidence for the long-term programming effects of early-life exposure to SSRIs on female offspring, particularily with regard to affect-related behaviors and their underlying molecular mechanisms.

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