• Title/Summary/Keyword: Brain-derived neurotrophic factor(BDNF)

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The Effects of Regular Taekwondo Exercise on Brain wave activation and Neurotrophic Factors in Undergraduate male students (16주간의 태권도 프로그램이 중년 비만 여성의 뇌신경성장인자 및 인지기능에 미치는 영향)

  • Ha, Min-Seong;Roh, Hee-Tae;Park, Hae-Chan;Cho, Su-Youn
    • Journal of the Korean Applied Science and Technology
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    • v.37 no.2
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    • pp.354-361
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    • 2020
  • The purpose of this study was to investigate the effects of regular taekwondo training on neurotrophic factors and cognitive function in obese middle-aged women. Thirty-three middle-aged women with obesity were selected for this study and randomly assigned into a control group(CG, n=18) and an taekwondo group(TG, n=15). The TG performed taekwondo training 5 times weekly for 16 weeks, while the CG did not exercise training. Serum brain-derived neurotrophic factor(BDNF), vascular endothelial growth factor(VEGF), and insulin-like growth factor-1(IGF-1) levels were analyzed and Stroop Color and Word tests were performed before and after the intervention. The serum BDNF and IGF-1 levels were significantly increased in the TG after the intervention(p<.05). On the other hand, no statistically significant differences were found in the serum VEGF levels, or in the Stroop Color and Word Test scores(p>.05). These results suggest that regular taekwondo training may be affects levels of peripheral neurotrophic factors but not cognitive function in obese middle-aged women.

Effects of Memory and Learning Training on Neurotropic Factor in the Hippocampus after Brain Injury in Rats (뇌손상 흰쥐에서 기억과 학습훈련이 해마의 신경 성장인자에 미치는 영향)

  • Heo, Myoung;Bang, Yoo-Soon
    • The Journal of the Korea Contents Association
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    • v.9 no.2
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    • pp.309-317
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    • 2009
  • This study was to investigate the effects of restoring cognition function and neurotrophic factor in the hippocampus according to memory and learning training in rats affected by brain injury. Brain injury was induced in Sprague-Dawley rats(36 rats) through middle cerebral artery occlusion(MCAo). And then experiment groups were randomly divided into three groups; Group I: Brain injury induction(n=12), Group II: the application for treadmill training after brain injury induction(n=12), Group III: the application for memory and learning training after brain injury induction(n=12). Morris water maze acquisition test and retention test were performed to test cognitive function. And the histological examination was also observed through the immunohistochemistric response of BDNF(brain-derived neurotrophic factor) in the hippocampus. For Morris water maze acquisition test, there were significant interactions among the groups with the time(p<.001). The time to find the circular platform in Group III was more shortened than in Group I, II on the 9th, 10th, 11th and 12th day. For Morris water maze retention test, there were significant differences among the groups(p<.001). The time to dwell on quadrant circular platform in Group III on the 13th day was the longest compared with other groups. And as the result of observing the immunohistochemistric response of BDNF in the hippocampus CA1, the response of immunoreactive positive in Group III on the 7th day increased more than that of Group I, II. These results suggested that the memory and learning training in rats with brain injury has a more significant impact on restoring cognitive function via the changes of neurotropic factor expression and synaptic neuroplasticity.

The Role of Job Stress and Brain-Derived Neurotrophic Factor Gene Polymorphism on the Severity of Alcohol Drinking in Korean Office Workers in Their Twenties (20대 한국 직장인의 음주 심각도에 대한 직무 스트레스와 BDNF 유전자 다형성의 역할)

  • Kim, Bo-Ah;Lee, Sang-Ick;Kim, Sie-Kyeong;Shin, Chul-Jin;Son, Jung-Woo;Hong, Joo-Bong;Nam, Yeong-Woo;Ju, Ga-Won
    • Korean Journal of Biological Psychiatry
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    • v.19 no.2
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    • pp.91-98
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    • 2012
  • Objectives : The aim of this study was to examine the effects of brain-derived neurotrophic factor (BDNF) genetic polymorphism and job stress on the severity of alcohol drinking. It was hypothesized that individuals with the Met/Met BDNF genotype would be more vulnerable than those carrying the Val allele. Methods : Participants were 133 healthy Korean adults (mean age $28.2{\pm}1.1$). Job stress and the severity index of drinking were investigated through self-reported questionnaires. BDNF (rs6265) gene was genotyped. Results : There was no significant association between job stress and the severity of alcohol drinking. Although the severity of alcohol drinking was not associated with BDNF genetic polymorphism, there was a significant difference in men according to genotype and job stress. Men with homozygous BDNF Met allele were more severe in alcohol drinking when job stress was high, less severe in alcohol drinking when job stress was low than those carrying the Val allele (F = 4.47, p = 0.038). Also higher level of job stress was correlated with higher severity of alcohol drinking in men homozygous for BDNF Met allele (rs = 0.620, p = 0.005). Conclusions : These findings suggest the possibility that Met allele could have differential susceptibility, with men homozygous for BDNF Met allele being more susceptible to both more adverse and less adverse environmental influences.

Nerve Growth Factor Activates Brain-derived Neurotrophic Factor Promoter IV via Extracellular Signal-regulated Protein Kinase 1/2 in PC12 Cells

  • Park, So Yun;Lee, Ji Yun;Choi, Jun Young;Park, Mae Ja;Kim, Dong Sun
    • Molecules and Cells
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    • v.21 no.2
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    • pp.237-243
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    • 2006
  • Brain-derived neurotrophic factor (BDNF) is a neuromodulator of nociceptive responses in the dorsal root ganglia (DRG) and spinal cord. BDNF synthesis increases in response to nerve growth factor (NGF) in trkA-expressing small and medium-sized DRG neurons after inflammation. Previously we demonstrated differential activation of multiple BDNF promoters in the DRG following peripheral nerve injury and inflammation. Using reporter constructs containing individual promoter regions, we investigated the effect of NGF on the multiple BDNF promoters, and the signaling pathway by which NGF activates these promoters in PC12 cells. Although all the promoters were activated 2.4-7.1-fold by NGF treatment, promoter IV gave the greatest induction. The p38 mitogen-activated protein kinase (MAPK) inhibitor, SB203580, phosphatidylinositol 3-kinase (PI-3K) inhibitor, LY294003, protein kinase A (PKA) inhibitor, H89, and protein kinase C (PKC) inhibitor, chelerythrine, had no effect on activation of promoter IV by NGF. However, activation was completely abolished by the MAPK kinase (MEK) inhibitors, U0126 and PD98059. In addition, these inhibitors blocked NGF-induced phosphorylation of extracellular signal-regulated protein kinase (ERK) 1/2. Taken together, these results suggest that the ERK1/2 pathway activates BDNF promoter IV in response to NGF independently of NGF-activated signaling pathways involving PKA and PKC.

BDNF Methylation and Suicidal Ideation in Patients with Acute Coronary Syndrome

  • Kang, Hee-Ju;Bae, Kyung-Yeol;Kim, Sung-Wan;Shin, Il-Seon;Hong, Young Joon;Ahn, Youngkeun;Jeong, Myung Ho;Yoon, Jin-Sang;Kim, Jae-Min
    • Psychiatry investigation
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    • v.15 no.11
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    • pp.1094-1097
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    • 2018
  • Objective Patients with acute coronary syndrome (ACS) are at an increased risk of suicide. It is well known that epigenetic mechanisms may explain the pathophysiology of suicidal behavior including suicidal ideation (SI), but no study has explored these mechanisms in ACS populations. Methods In total, 969 patients were initially recruited within 2 weeks of the acute coronary event and, 711 patients were successfully followed up 1 year after ACS. SI was evaluated using the relevant items on the Montgomery-${\AA}sberg$ Depression Rating Scale and covariates potentially affecting SI were estimated. Results Brain-derived neurotrophic factor (BDNF) hypermethylation was associated with SI in both the acute and chronic phases of ACS, although the association was not statistically significant in the acute phase after applying Bonferroni's correction. Conclusion These results suggested that BDNF hypermethylation may have played a role in an epigenetic predisposition for SI in ACS patients, particularly during the chronic phase.

Alcohol exposure induces depression-like behavior by decreasing hippocampal neuronal proliferation through inhibition of the BDNF-ERK pathway in gerbils

  • Kim, Ji-Eun;Ji, Eun-Sang;Seo, Jin-Hee;Lee, Moon-Hyoung;Cho, Se-Hyung;KimPak, Young-Mi;Seo, Tae-Beom;Kim, Chang-Ju
    • Animal cells and systems
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    • v.16 no.3
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    • pp.190-197
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    • 2012
  • Depression is one of the most prevalent diseases of alcohol abuse. Brain-derived neurotrophic factor (BDNF) plays a critical role in cell survival in the hippocampus. Phosphorylation of extracellular signal-regulated kinase 1/2 (p-ERK1/2) is induced by BDNF, and it regulates cell proliferation and differentiation in the brain. We investigated the effects of alcohol intake on depression-like behavior, cell proliferation, expressions of BDNF and its downstream molecules in the hippocampus using Mongolian gerbils. The gerbils were divided into four groups: control group, 0.5 g/kg alcohol-treated group, 1 g/kg alcohol-treated group, 2 g/kg alcohol-treated group. Each dose of alcohol was orally administered for 3 weeks. The present results demonstrated that alcohol intake induced depression-like behavior. Both 5-hydroxytryptamine synthesis and its synthesizing enzyme tryptophan hydroxylase expression in the dorsal raphe and cell proliferation in the hippocampal dentate gyrus were decreased by alcohol intake. Alcohol intake suppressed BDNF expression, and resulted in the decrease of its downstream molecules, pERK1/2 and Bcl-2, in the hippocampus. We showed that alcohol intake may lead to a depressed-like state with reduced hippocampal cell proliferation through inhibition of the BDNF-ERK signaling pathway.

Expression of Neurotrophic Factors and Their Receptors in Rat Posterior Taste Bud Cells

  • Park, Dong-Il;Chung, Ki-Myung;Cho, Young-Kyung;Kim, Kyung-Nyun
    • International Journal of Oral Biology
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    • v.39 no.2
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    • pp.107-114
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    • 2014
  • Taste is an important sense in survival and growth of animals. The growth and maintenance of taste buds, the receptor organs of taste sense, are under the regulation of various neurotrophic factors. But the distribution aspect of neurotrophic factors and their receptors in distinct taste cell types are not clearly known. The present research was designed to characterize mRNA expression pattern of neurotrophic factors and their receptors in distinct type of taste cells. In male 45-60 day-old Sprague-Dawley rats, epithelial tissues with and without circumvallate and folliate papillaes were dissected and homogenized, and mRNA expressions for neurotrophic factors and their receptors were determined by RT-PCR. The mRNA expressions of brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT3), receptor tyrosine kinase B (TrkB), exclusion of nerve growth factor (NGF), neurotrophin-4/5 (NT4/5), receptor tyrosine kinase A (TrkA), receptor tyrosine kinase C (TrkC), and p75NGFR were observed in some population of taste cell. In support of this result and to characterize which types of taste cells express NT3, BDNF, or TrkB, we examined mRNA expressions of NT3, BDNF, or TrkB in the $PLC{\beta}2$ (a marker of Type II cell)-and/or SNAP25 (a marker of Type III cell)-positive taste cells by a single taste cell RT-PCR and found that the ratio of positively stained cell numbers were 17.4, 6.5, 84.1, 70.3, and 1.4 % for $PLC{\beta}2$, SNAP25, NT3, BDNF, and TrkB, respectively. In addition, all of $PLC{\beta}2$-and SNAP25-positive taste cells expressed NT3 mRNA, except for one taste bud cell. The ratios of NT3 mRNA expressions were 100% and 91.7% in the SNAP25-and $PLC{\beta}2$-positive taste cells, respectively. However, two TrkB-positive taste cells co-expressed neither $PLC{\beta}2$ nor SNAP 25. The results suggest that the most of type II or type III cells express BDNF and NT3 mRNA, but the expression is shown to be less in type I taste cells.

Exploring amygdala structural changes and signaling pathways in postmortem brains: consequences of long-term methamphetamine addiction

  • Zahra Azimzadeh;Samareh Omidvari;Somayeh Niknazar;Saeed Vafaei-Nezhad;Navid Ahmady Roozbahany;Mohammad-Amin Abdollahifar;Foozhan Tahmasebinia;Gholam-Reza Mahmoudiasl;Hojjat Allah Abbaszadeh;Shahram Darabi
    • Anatomy and Cell Biology
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    • v.57 no.1
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    • pp.70-84
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    • 2024
  • Methamphetamine (METH) can potentially disrupt neurotransmitters activities in the central nervous system (CNS) and cause neurotoxicity through various pathways. These pathways include increased production of reactive nitrogen and oxygen species, hypothermia, and induction of mitochondrial apoptosis. In this study, we investigated the long-term effects of METH addiction on the structural changes in the amygdala of postmortem human brains and the involvement of the brain- cAMP response element-binding protein/brain-derived neurotrophic factor (CREB/BDNF) and Akt-1/GSK3 signaling pathways. We examined ten male postmortem brains, comparing control subjects with chronic METH users, using immunohistochemistry, real-time polymerase chain reaction (to measure levels of CREB, BDNF, Akt-1, GSK3, and tumor necrosis factor-α [TNF-α]), Tunnel assay, stereology, and assays for reactive oxygen species (ROS), glutathione disulfide (GSSG), and glutathione peroxidase (GPX). The findings revealed that METH significantly reduced the expression of BDNF, CREB, Akt-1, and GPX while increasing the levels of GSSG, ROS, RIPK3, GSK3, and TNF-α. Furthermore, METH-induced inflammation and neurodegeneration in the amygdala, with ROS production mediated by the CREB/BDNF and Akt-1/GSK3 signaling pathways.

In Vitro Neural Cell Differentiation Derived from Human Embryonic Stem Cells: II. Generation of Specific Neurons from Neural Progenitor Cells Treated with BDNF and PDGF

  • Jo Hyeon-Jeong;Kim Eun-Yeong;Choe Gyeong-Hui;An So-Yeon;Park Se-Pil;Im Jin-Ho
    • Proceedings of the KSAR Conference
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    • 2002.06a
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    • pp.84-84
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    • 2002
  • This study was to investigate generation of the specific neuronal cell in vitro from the neural progenitors derived from human embryonic stem (hES, MB03) cells. For the neural progenitor cell formation, we produced embryoid bodies (EB: for 5 days, without mitogen) from hES cells and then neurospheres (for 7-10 days, 20 ng/㎖ of bFGF added N2 medium) from EB. And then for the differentiation into neuronal cells, neural progenitor cells were cultured in N2 medium (without bFGF) supplemented with brain derived neurotrophic factor (BDNF, 5 ng/㎖) or platelet derived growth factor-bb (pDGF-bb, 20ng/㎖) for 2 weeks. (omitted)

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Exercise and Neuroplasticity: Benefits of High Intensity Interval Exercise (운동과 뇌신경가소성: 고강도 인터벌 운동의 효과성 고찰)

  • Hwang, Ji Sun;Kim, Tae Young;Hwang, Moon-Hyon;Lee, Won Jun
    • Journal of Life Science
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    • v.26 no.1
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    • pp.129-139
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    • 2016
  • Exercise increases the expression and interaction of major neurotrophic factors such as brain-derived neurotrophic factor (BDNF), insulin-like growth factor-1 (IGF-1), and vascular endothelial growth factor (VEGF) at both central and peripheral tissues, which contributes to improved brain and neural plasticity and cognitive function. Previous findings have been to understand the effect of light or moderate intensity aerobic exercise on neurotrophic factors and cognitive function, not that of high intensity aerobic exercise. However, recent findings suggest that high intensity interval training is a safe, less time-consuming, efficient way to improve cardiorespiratory fitness and weight control, thus American College of Sport Medicine (ACSM)’s guidelines for exercise prescription for various adult populations also recommend the application of high intensity interval training to promote their overall health. High intensity interval training also enhances the expression of BDNF, IGF-1, and VEGF at the brain and peripheral tissues, which improves cognitive function. Increased frequency of intermittent hypoxia and increased usage of lactate as a supplementary metabolic resource at the brain and neural components are considered a putative physiological mechanism by which high intensity interval training improves neurotrophic factors and cognitive function. Therefore, future studies are required to understand how increased hypoxia and lactate usage leads to the improvement of neurotrophic factors and what the related biological mechanisms are. In addition, by comparing with the iso-caloric moderate continuous exercise, the superiority of high intensity interval training on the expression of neurotrophic factors and cognitive function should be demonstrated by associated future studies.