• 제목/요약/키워드: Brain-derived neurotrophic factor (BDNF)

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

  • 하민성;노희태;박해찬;조수연
    • 한국응용과학기술학회지
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    • 제37권2호
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    • pp.354-361
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    • 2020
  • 본 연구는 규칙적인 태권도 트레이닝이 비만 중년 여성의 뇌신경성장인자 및 인지기능에 미치는 영향을 알아보는데 목적이 있었다. 본 연구를 위하여 중년 비만 여성 33명이 연구대상자로 선정되었으며, 연구대상자들은 태권도 그룹(TG, n=15)과 대조그룹(CG, n=18)에 무선 배정되었다. 태권도 그룹은 16주간 일주일에 5번 태권도 트레이닝을 실시하였으며, 두 그룹 모두 트레이닝 전과 후 각각 brain-derived neurotrophic factor(BDNF), vascular endothelial growth factor(VEGF), insulin-like growth factor-1(IGF-1) 농도 검사와 Stroop Color and Word test를 실시하였다. 연구 결과 태권도 그룹의 BDNF와 IGF-1이 트레이닝 후 유의하게 증가한(p<.05) 반면 VEGF와 Stroop Color and Word Test 결과는 유의한 차이가 나타나지 않아 규칙적인 태권도 트레이닝이 비만 중년 여성의 뇌신경영양인자에는 긍정적이지만 뇌 인지기능에는 영향이 없는 것으로 나타났다.

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

  • 허명;방요순
    • 한국콘텐츠학회논문지
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    • 제9권2호
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    • pp.309-317
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    • 2009
  • 본 연구는 뇌손상 흰쥐에서 기억과 학습훈련을 통해 인지기능회복과 해마의 신경 성장인자에 미치는 영향을 알아보고자 하였다. 뇌손상은 Sprague-Dawley계 흰쥐 36마리를 중대뇌동맥(middle cerebral artery)을 폐색하여 유발하였고, 실험 군들은 3개 군으로 분류하였다; 실험 군 I은 뇌손상유발 군(n=12), 실험 군 II는 뇌손상 유발 후 트레드밀훈련 군(n=12), 실험 군 Ⅲ은 뇌손상 유발 후 기억과 학습훈련 군(n=12)으로 나누었다. 인지기능 검사를 위해 수중모리스미로 습득검사와 파지검사를 실시하였으며, 조직학적 검사는 해마조직의 BDNF(brain-derived neurotrophic factor) 면역조직화학 반응을 관찰하였다. 수중모리스미로 습득 검사(Morris water maze acquisition test)는 시간과 군사이의 교호작용이 유의한 차이가 나타났고(p<.001), III군에서 9일에서 12일째까지 원형도피대를 찾는 시간이 I, II군에 비해 단축되었다. 수중모리스미로 파지검사(retention test)는 군 사이에서도 유의한 차이가 나타났으며(p<.001), 13일째 III군에서 원형도피대가 있었던 사분원에 배회하는 시간이 가장 길었다. 조직학적 검사는 III군에서 7일째 해마조직의 CA1에서 BDNF의 면역조직화학반응이 I, II군에 비해 면역양성반응의 증가를 관찰하였다. 뇌손상 흰쥐에서 기억과 학습훈련이 신경성장인자 발현 변화와 이로 인한 신경연접 가소성의 변화를 통해 인지기능회복에 더 좋은 영향을 주었다.

20대 한국 직장인의 음주 심각도에 대한 직무 스트레스와 BDNF 유전자 다형성의 역할 (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)

  • 김보아;이상익;김시경;신철진;손정우;홍주봉;남영우;주가원
    • 생물정신의학
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    • 제19권2호
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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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    • 제21권2호
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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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    • 제15권11호
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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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    • 제16권3호
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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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    • 제39권2호
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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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    • 제57권1호
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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
    • 한국동물번식학회:학술대회논문집
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    • 한국동물번식학회 2002년도 춘계학술발표대회 발표논문초록집
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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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운동과 뇌신경가소성: 고강도 인터벌 운동의 효과성 고찰 (Exercise and Neuroplasticity: Benefits of High Intensity Interval Exercise)

  • 황지선;김태영;황문현;이원준
    • 생명과학회지
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    • 제26권1호
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    • pp.129-139
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    • 2016
  • 운동은 중추와 말초의 각종 성장인자(BDNF, IGF-1, VEGF)들의 상호작용에 의해 뇌신경가소성을 증진시키고 인지기능을 향상시킨다. 지금까지 저·중강도 지속성 유산소 운동의 효과를 검증하는 선행연구가 주로 이루어졌기 때문에 고강도 운동에 따른 뇌신경성장인자의 발현 및 인지기능 개선 효과에 대한 연구는 미흡한 실정이다. 하지만 최근의 과학적 증거들은 고강도 인터벌 운동이 시간 효율성, 안전성, 심폐지구력 개선 및 체중 감소에 효과적임을 암시하고 있으며, 미스포츠의학회(ACSM)에서 권장하는 일반인을 위한 운동지침에서도 무리가 되지 않는 수준에서 고강도 인터벌 운동 수행을 강조하고 있다. 특히 최근에 발표된 선행 연구에서 고강도 인터벌 운동은 말초조직과 뇌에서의 BDNF, IGF-1, VEGF의 발현을 증가시키고 그로 인한 인지기능 발달에 기여한다는 것을 보고하였으며, 관련된 유력한 생리학적 기전으로 고강도 인터벌 운동으로 인한 뇌의 저산소화와 뇌신경대사의 부가적인 에너지원이 될 수 있는 젖산 이용성 증가가 대두되고 있다. 따라서 향후 저산소화 및 젖산 이용성 증가에 따른 뇌신경성장인자 발현 개선에 어떤 분자생물학적 기전이 관여하는지를 탐구할 필요가 있으며, 또한 동일한 운동량을 가진 저·중강도 지속성 유산소 운동과의 비교 연구를 통해 뇌신경성장인자의 발현 및 인지기능 개선에 있어 고강도 인터벌 운동의 우수성을 입증하는 연구가 요구된다.