Yukiko Ishibashi, N. Izumo, K. Iwata, Tomomi Morikawa, T. Kameyama, Yasuo Watanabe, T. Manabe, Hideo Matsuzaki
Studies suggest that increased expression of brain-derived neurotrophic factor (BDNF) could mediate the antidepressant effects of drugs. We analyzed the effects of fluvoxamine on locomotor activities, serotonin levels in the amygdala, and hippocampal expression of BDNF mRNA in ovariectomized (OVX) rats. Female Wistar rats (8 weeks, 180–200 g) were divided into four groups: sham; OVX; OVX with estrogen; and OVX with fluvoxamine. Six weeks after ovariectomy, rats were assessed according to spontaneous locomotor activity, forced-swimming test (FST), and microdialyses experiments. Body and uterine weight of OVX rats 6 weeks after surgery were significantly increased and decreased, respectively, compared with those of the sham group, but these changes were returned to sham-group levels upon chronic administration of estrogen and fluvoxamine. More potent decreases in voluntary activities were observed in OVX rats compared with rats in the sham group, but were increased markedly upon administration of estrogen and fluvoxamine. In the FST, immobility time and beat counts were increased and decreased significantly by ovariectomy compared with those of the sham group, respectively, but estrogen and fluvoxamine treatment reversed these changes significantly. More potent decreases in serotonin release in the amygdala were observed in OVX rats compared with those of sham rats, but were reversed upon estrogen Journal of Brain Science, June 30, 2016,Vol.46 7 replacement. Similar recovery was observed in OVX rats upon fluvoxamine treatment. These data suggest that, in OVX rats, chronic administration of fluvoxamine can recover estrogen-dependent changes in behaviors, decreased serotonin release in the amygdala, and reduced expression of BDNF mRNA. Key wards: Amygdala, Serotonin, Estrogen, Fluvoxamine, OVX; Abbreviations BDNF, brain-derived neurotrophic factor; ER, endoplasmic reticulum; OVX, ovariectmized; RT-PCR, reverse transcription-polymerase chain reaction; SSRI, selective serotonin reuptake inhibitor; XBP-1, X-box binding protein-1; mRNA, messenger ribonucleic acid Introduction The female hormone estrogen has an important role in bone physiology (reviewed in [15, 16]). Moreover, there is a close relationship between estrogen and memory, learning, and emotion in the brain (reviewed in [16]). Also, it has been reported that replenishment with estrogen can improve recognition, learning and memory (reviewed in [3, 5, 14]). We reported that, in female rats 6 weeks after their ovaries had been removed, depression-like symptoms (as manifested by decreases in spontaneous locomotor activities and serotonin levels in the amygdala) could be observed [9]. Depression is a complex disorder brought about by genetic and environmental conditions. Depression involves brain abnormalities as well as dysfunction of the endocrine system, inflammation, altered glucose metabolism and, in some cases, coronary artery disease [8, 18]. Selective serotonin reuptake inhibitors (SSRIs)
研究表明,脑源性神经营养因子(BDNF)的表达增加可能介导药物的抗抑郁作用。我们分析了氟伏沙明对去卵巢(OVX)大鼠运动活动、杏仁核血清素水平和海马BDNF mRNA表达的影响。雌性Wistar大鼠(8周,180 ~ 200 g)分为4组:假手术组;OVX;OVX加雌激素;用氟伏沙明和OVX切除卵巢6周后,根据自主运动活动、强迫游泳试验(FST)和微透析实验对大鼠进行评估。术后6周,OVX大鼠的体重和子宫重量分别较假手术组明显增加和减少,但经长期给予雌激素和氟伏沙明后,这些变化又恢复到假手术组的水平。与假手术组的大鼠相比,OVX大鼠的自愿活动明显减少,但在给予雌激素和氟伏沙明后明显增加。在FST中,与假手术组相比,卵巢切除术后静止时间和心跳计数分别显著增加和减少,但雌激素和氟伏沙明治疗可显著逆转这些变化。与假手术大鼠相比,OVX大鼠杏仁核中血清素释放的减少更明显,但在雌激素作用下则相反。46 .更换。在氟伏沙明治疗的OVX大鼠中也观察到类似的恢复。这些数据表明,在OVX大鼠中,长期给予氟伏沙明可以恢复雌激素依赖的行为改变,减少杏仁核中血清素的释放,降低BDNF mRNA的表达。关键词:杏仁核,血清素,雌激素,氟伏沙明,OVX;脑源性神经营养因子;内质网;OVX ovariectmized;逆转录聚合酶链反应;选择性血清素再摄取抑制剂;XBP-1, X-box结合蛋白1;雌性激素雌激素在骨生理中具有重要作用(综述于[15,16])。此外,雌激素与大脑中的记忆、学习和情绪之间存在密切关系(见b[16])。此外,有报道称补充雌激素可以改善认知、学习和记忆(参见[3,5,14])。我们报道,在雌性大鼠卵巢切除6周后,可以观察到抑郁样症状(表现为自发运动活动和杏仁核血清素水平下降)[9]。抑郁症是一种由遗传和环境条件引起的复杂疾病。抑郁症包括脑异常以及内分泌系统功能障碍、炎症、葡萄糖代谢改变,在某些情况下还包括冠状动脉疾病[8,18]。选择性血清素再摄取抑制剂(SSRIs)是治疗抑郁症和抑郁样症状的一线药物。然而,抗抑郁药的耐药性已被证实,因此需要开发具有新的作用机制的新药物。脑科学杂志,2016年6月30日,卷。研究表明,脑源性神经营养因子(BDNF)信号传导对于抗抑郁药物[20]的作用是必要和充分的。BDNF信号通路与单磷酸环腺苷反应元件结合蛋白相关,可诱导神经发生[20]。此外,在患有抑郁症的人的死后海马样本中观察到高水平的BDNF。这些发现表明BDNF表达减少与抑郁症发病之间存在相关性。此外,最近的一份报告表明,SSRI氟伏沙明通过长期注射地塞米松逆转了表现出抑郁样行为的小鼠BDNF信使核糖核酸(mRNA)表达的减少。因此,抗抑郁药物的治疗效果可能是通过BDNF表达增加介导的。在本研究中,我们分析了抗抑郁药氟伏沙明对去卵巢(OVX)大鼠运动活动、杏仁核血清素水平和海马BDNF mRNA表达的慢性(6周)影响。材料与方法研究方案的伦理批准本研究方案经横滨药学院(神奈川,日本)伦理委员会批准。所有动物实验均根据日本药理学会批准的《实验动物护理和使用指南》(美国国立卫生研究院Bethesda, MD, USA)进行。动物、卵巢切除和药物管理动物护理和卵巢切除与前面描述的一样,只是做了一些修改。将36只雌性Wistar大鼠(8周,180 ~ 200 g)分为4组,每组9只。 实验开始前,让大鼠适应环境≥1周(12 h明暗循环;脑科学杂志,2016年6月30日,卷。(早上7点开,晚上7点关)。1周后,如前所述进行OVX和假手术(Fukushima et al., 2000)。卵巢切除术后1周,氟伏沙明(50 mg/kg体重;Wako Pure Chemical Industries,大阪,日本)和β-雌二醇(50 μg/kg体重;Sigma-Aldrich, st . Louis, MO, USA)每周给药5次(分别为p.o.和i.p.),持续6周。卵巢切除术后6周,根据自主运动活动、FST和微透析实验对大鼠进行评估,如前所述[9,17]。定量逆转录聚合酶链反应(RT-PCR) RT-PCR按照先前描述的方法进行。统计分析按前面所述进行统计分析。结果OVX大鼠术后6周体重与假手术组比较,体重明显增加,子宫重量明显减少(图1a、b;sham组和OVX组)。长期给药后,OVX大鼠的体重增加和子宫重量减少恢复到假组水平(图1a和b;假手术组和雌激素组)。在体重和子宫重量的增加和减少方面,慢性服用氟伏沙明有恢复的趋势,但差异不显著(图1a和b;假手术组和氟伏沙明组)。图2a显示了卵巢切除6周后四组在黑暗期(晚上7点至早上7点)12小时的自发运动活动。与假手术组相比,OVX大鼠的自愿活动减少更明显(图2b)。《脑科学杂志》,2016年6月30日,卷。46 10数据与我们之前的报告b[9]相似。在雌激素和氟伏沙明的作用下,OVX大鼠在暗期运动活动的减少明显增加(图2b)。接下来,我们分析了四组大鼠FST的静止时间和心跳计数(图3)。与假手术组相比,卵巢切除术后静止时间和心跳计数分别显著增加和减少(图3a和b;sham组和OVX组)。这些数据与我们之前的报告b[9]一致。雌激素和氟伏沙明治疗使这些变化明显逆转到对照大鼠的水平(图3a和b)。接下来,我们分析了相同条件下杏仁核中的血清素水平(图4)。与假手术大鼠相比,OVX大鼠杏仁核中血清素释放的减少更明显(图4a)。这些观察结果与我们以前的报告b[9]一致。在雌激素替代后,杏仁核中血清素水平的下降被逆转(图4a;卵巢切除术后血清素水平的降低依赖于雌激素的消失。在氟伏沙明治疗的OVX大鼠中观察到类似的恢复(图4a;OVX和氟伏沙明)。然而,在杏仁核多巴胺释放的情况下,没有检测到血清素释放的恢复(图4b)。这一结果是意料之中的,因为SSRIs具有针对血清素的特异性作用机制。接下来,我们使用RT-PCR分析假手术大鼠和OVX大鼠的海马BDNF表达(图5)。从大脑皮层或脑干获得的任何组的样本均未观察到显著变化(图5;中下面板)。与sham组相比,OVX组海马BDNF表达的下降更明显。46 11组(图5;上半部分)。这种BDNF表达的升高在雌激素治疗后明显恢复(图5;上半部分)。经氟伏沙明治疗后,OVX大鼠海马BDNF表达显著恢复(图5;上半部分)。各组海马雌激素受体-1基因表达均无变化(数据未显示)。本研究显示,卵巢切除6周后,OVX大鼠的体重和子宫重量分别较假手术组明显增加和减少(图1),这一现象与文献报道一致[1,4,9]。这些结果表明我们成功地进行了卵巢切除术。长期给药后,OVX大鼠体重的增加和子宫重量的减少恢复到假组水平(图1),表明OVX大鼠体重的增加明显依赖于雌激素的消失。 此外,在长期服用氟伏沙明后,体重和子宫重量的增加和减少也有恢复的趋势,但差异不显著(图2)。
{"title":"Fluvoxamine reverses estrogen-dependent decline in voluntary activities and decreased amygdala levels of serotonin in ovariectomized rats","authors":"Yukiko Ishibashi, N. Izumo, K. Iwata, Tomomi Morikawa, T. Kameyama, Yasuo Watanabe, T. Manabe, Hideo Matsuzaki","doi":"10.20821/JBS.46.0_5","DOIUrl":"https://doi.org/10.20821/JBS.46.0_5","url":null,"abstract":"Studies suggest that increased expression of brain-derived neurotrophic factor (BDNF) could mediate the antidepressant effects of drugs. We analyzed the effects of fluvoxamine on locomotor activities, serotonin levels in the amygdala, and hippocampal expression of BDNF mRNA in ovariectomized (OVX) rats. Female Wistar rats (8 weeks, 180–200 g) were divided into four groups: sham; OVX; OVX with estrogen; and OVX with fluvoxamine. Six weeks after ovariectomy, rats were assessed according to spontaneous locomotor activity, forced-swimming test (FST), and microdialyses experiments. Body and uterine weight of OVX rats 6 weeks after surgery were significantly increased and decreased, respectively, compared with those of the sham group, but these changes were returned to sham-group levels upon chronic administration of estrogen and fluvoxamine. More potent decreases in voluntary activities were observed in OVX rats compared with rats in the sham group, but were increased markedly upon administration of estrogen and fluvoxamine. In the FST, immobility time and beat counts were increased and decreased significantly by ovariectomy compared with those of the sham group, respectively, but estrogen and fluvoxamine treatment reversed these changes significantly. More potent decreases in serotonin release in the amygdala were observed in OVX rats compared with those of sham rats, but were reversed upon estrogen Journal of Brain Science, June 30, 2016,Vol.46 7 replacement. Similar recovery was observed in OVX rats upon fluvoxamine treatment. These data suggest that, in OVX rats, chronic administration of fluvoxamine can recover estrogen-dependent changes in behaviors, decreased serotonin release in the amygdala, and reduced expression of BDNF mRNA. Key wards: Amygdala, Serotonin, Estrogen, Fluvoxamine, OVX; Abbreviations BDNF, brain-derived neurotrophic factor; ER, endoplasmic reticulum; OVX, ovariectmized; RT-PCR, reverse transcription-polymerase chain reaction; SSRI, selective serotonin reuptake inhibitor; XBP-1, X-box binding protein-1; mRNA, messenger ribonucleic acid Introduction The female hormone estrogen has an important role in bone physiology (reviewed in [15, 16]). Moreover, there is a close relationship between estrogen and memory, learning, and emotion in the brain (reviewed in [16]). Also, it has been reported that replenishment with estrogen can improve recognition, learning and memory (reviewed in [3, 5, 14]). We reported that, in female rats 6 weeks after their ovaries had been removed, depression-like symptoms (as manifested by decreases in spontaneous locomotor activities and serotonin levels in the amygdala) could be observed [9]. Depression is a complex disorder brought about by genetic and environmental conditions. Depression involves brain abnormalities as well as dysfunction of the endocrine system, inflammation, altered glucose metabolism and, in some cases, coronary artery disease [8, 18]. Selective serotonin reuptake inhibitors (SSRIs) ","PeriodicalId":15186,"journal":{"name":"Journal of Behavioral and Brain Science","volume":"24 1","pages":"5-19"},"PeriodicalIF":0.0,"publicationDate":"2016-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78425594","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
M. Ikuma, Y. Ouchi, Kyoko Nakaizumi, Masamichi Yokokura, K. Takebayashi, Katsuaki Suzuki, N. Mori
Background: Accumulating evidence suggests that microglia cells contribute to the normal brain homeostasis in addition to working as immune-competent cells in pathological processes associated with neurodegeneration or neuroinflammation. Microglial activation can be measured in vivo using 11C-(R)-PK11195 and positron emission tomography (PET). The aim of the study was to determine possible relationships between microglial activation and age as well as cognitive functioning in healthy Journal of Brain Science, June 30, 2016,Vol.46 56 subjects. Methods: Fifty-five healthy subjects (male/female = 35/20, age range 18-84 years) underwent a PET measurement with 11C-(R)-PK11195 and T1-weighted magnetic resonance imaging (MRI). A subset of young male subjects (age range 21-40 years) were assessed their intelligence quotient (IQ) using the third edition of Wechsler adult intelligence scale within the same day. The binding potentials of 11C-(R)-PK11195 in selected brain regions were estimated by a modified simplified reference tissue model in each of subjects. Results: Bindings of 11C-(R)-PK11195 in the cerebral cortices and subcortical regions significantly and positively correlated with age of subjects. When each sex was separately analyzed, the significant positive correlation was observed in male, but not female, subjects. In a subset of young male subjects, there was a negative correlation between the IQ scores and regional 11C-(R)-PK11195 bindings in cortical and subcortical regions. Conclusion: Results suggest that microglial activation in the brain might be associated with not only normal aging but also cognitive functioning in the youth.
{"title":"Microglial activation in healthy adult Japanese subjects: apositron emission tomography study","authors":"M. Ikuma, Y. Ouchi, Kyoko Nakaizumi, Masamichi Yokokura, K. Takebayashi, Katsuaki Suzuki, N. Mori","doi":"10.20821/JBS.46.0_55","DOIUrl":"https://doi.org/10.20821/JBS.46.0_55","url":null,"abstract":"Background: Accumulating evidence suggests that microglia cells contribute to the normal brain homeostasis in addition to working as immune-competent cells in pathological processes associated with neurodegeneration or neuroinflammation. Microglial activation can be measured in vivo using 11C-(R)-PK11195 and positron emission tomography (PET). The aim of the study was to determine possible relationships between microglial activation and age as well as cognitive functioning in healthy Journal of Brain Science, June 30, 2016,Vol.46 56 subjects. Methods: Fifty-five healthy subjects (male/female = 35/20, age range 18-84 years) underwent a PET measurement with 11C-(R)-PK11195 and T1-weighted magnetic resonance imaging (MRI). A subset of young male subjects (age range 21-40 years) were assessed their intelligence quotient (IQ) using the third edition of Wechsler adult intelligence scale within the same day. The binding potentials of 11C-(R)-PK11195 in selected brain regions were estimated by a modified simplified reference tissue model in each of subjects. Results: Bindings of 11C-(R)-PK11195 in the cerebral cortices and subcortical regions significantly and positively correlated with age of subjects. When each sex was separately analyzed, the significant positive correlation was observed in male, but not female, subjects. In a subset of young male subjects, there was a negative correlation between the IQ scores and regional 11C-(R)-PK11195 bindings in cortical and subcortical regions. Conclusion: Results suggest that microglial activation in the brain might be associated with not only normal aging but also cognitive functioning in the youth.","PeriodicalId":15186,"journal":{"name":"Journal of Behavioral and Brain Science","volume":"47 1","pages":"55-69"},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86703227","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Influence of unbalanced large head on neurodevelopment in infancy: a longitudinal birth cohort study","authors":"R. Oshima, K. Tsuchiya, N. Mori, N. Takei","doi":"10.20821/JBS.46.0_34","DOIUrl":"https://doi.org/10.20821/JBS.46.0_34","url":null,"abstract":"","PeriodicalId":15186,"journal":{"name":"Journal of Behavioral and Brain Science","volume":"27 1","pages":"34-54"},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83532990","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Placenta-derived hypo-serotonin situations in the developing forebrain inhibits dopaminergic fiber development, resulting in ADHD","authors":"Kohji Sato","doi":"10.20821/JBS.46.0_20","DOIUrl":"https://doi.org/10.20821/JBS.46.0_20","url":null,"abstract":"","PeriodicalId":15186,"journal":{"name":"Journal of Behavioral and Brain Science","volume":"101 1","pages":"20-33"},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73329844","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2015-10-01Epub Date: 2015-10-27DOI: 10.4236/jbbs.2015.511049
Taryn G Aubrecht, Zachary M Weil, Bachir Abi Salloum, Maria Eugenia Ariza, Marshall Williams, Brenda Reader, Ronald Glaser, John Sheridan, Randy J Nelson
Most adult humans have been infected with Epstein-Barr virus (EBV), which is thought to contribute to the development of chronic fatigue syndrome. Stress is known to influence the immune system and can exacerbate the sickness response. Although a role for psychological stress in the sickness response, particularly in combination with EBV-encoded deoxyuridine triphosphate nucleotidohydrolase (dUTPase) has been established, and the role of physical stressors in these interactions remains unspecified. In this study, we seek to determine the interaction of chronic physical (swim) stress and EBV-encoded dUTPase injection. We hypothesize that a chronic physical stressor will exacerbate the sickness response following EBV-encoded dUTPase injection. To test this hypothesis mice receive daily injections of EBV-encoded dUTPase or vehicle and are subjected to 15 min of swim stress each day for 14 days or left unmanipulated. On the final evening of injections mice undergo behavioral testing. EBV-encoded dUTPase injection alone produces some sickness behaviors. The physical swimming stress does not alter the sickness response.
{"title":"Chronic Physical Stress Does Not Interact with Epstein-Barr Virus (EBV)-Encoded Dutpase to Alter the Sickness Response.","authors":"Taryn G Aubrecht, Zachary M Weil, Bachir Abi Salloum, Maria Eugenia Ariza, Marshall Williams, Brenda Reader, Ronald Glaser, John Sheridan, Randy J Nelson","doi":"10.4236/jbbs.2015.511049","DOIUrl":"https://doi.org/10.4236/jbbs.2015.511049","url":null,"abstract":"<p><p>Most adult humans have been infected with Epstein-Barr virus (EBV), which is thought to contribute to the development of chronic fatigue syndrome. Stress is known to influence the immune system and can exacerbate the sickness response. Although a role for psychological stress in the sickness response, particularly in combination with EBV-encoded deoxyuridine triphosphate nucleotidohydrolase (dUTPase) has been established, and the role of physical stressors in these interactions remains unspecified. In this study, we seek to determine the interaction of chronic physical (swim) stress and EBV-encoded dUTPase injection. We hypothesize that a chronic physical stressor will exacerbate the sickness response following EBV-encoded dUTPase injection. To test this hypothesis mice receive daily injections of EBV-encoded dUTPase or vehicle and are subjected to 15 min of swim stress each day for 14 days or left unmanipulated. On the final evening of injections mice undergo behavioral testing. EBV-encoded dUTPase injection alone produces some sickness behaviors. The physical swimming stress does not alter the sickness response.</p>","PeriodicalId":15186,"journal":{"name":"Journal of Behavioral and Brain Science","volume":"5 11","pages":"513-523"},"PeriodicalIF":0.0,"publicationDate":"2015-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4862656/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34481287","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Y. Miyatake, S. Matsuzaki, M. Taniguchi, Hironori Takamura, Kohei Yamada, T. Hattori, T. Kameyama, T. Manabe, M. Tohyama, T. Katayama
{"title":"Identification and characterization of a novel splice variant of disrupted in schizophrenia 1 (Disc1)","authors":"Y. Miyatake, S. Matsuzaki, M. Taniguchi, Hironori Takamura, Kohei Yamada, T. Hattori, T. Kameyama, T. Manabe, M. Tohyama, T. Katayama","doi":"10.20821/JBS.45.0_5","DOIUrl":"https://doi.org/10.20821/JBS.45.0_5","url":null,"abstract":"","PeriodicalId":15186,"journal":{"name":"Journal of Behavioral and Brain Science","volume":"1 1","pages":"5-34"},"PeriodicalIF":0.0,"publicationDate":"2015-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83043752","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
45 Review The pathogenesis and clinical features of cerebrovascular disease in diabetes mellitus Jinlong Cheng1, Bolin Chen2,* 1. Department of Internal medicine , Tianjin MingJin metabolic disease hospital, Tianjin 300381,China 2. Department of Physiology and Pathophysiology, Tianjin Medical University Tianjin 300070, China * Correspondence to Bolin Chen E-mail: econversation@163.com Received:2015-02-01 Accepted:2015-03-01 Abstract Cerebrovascular disease is a kind of complications in diabetes mellitus which is induced by suger, fat and protein metabolic disorder. These series of nutrient metabolic disorder can lead to intracranial large blood vessels and microvascular lesions. About 20-40 percent of type 2 diabetes patients will suffer from cerebrovascular diseases which become the main causes of death in diabetic patients [1]. Recently many kinds of pathogenesis have been found by researchers about cerebrovascular diseases in diabetes mellitus such as hyperglycemia, insulin resistance [2], endothelial cell dysfunction [3], abnormal lipids metabolism and so on. The major clinical manifestations of diabetic cerebrovascular diseases are asymptomatic cerebral atherosclerosis, stroke, cerebral small vessel diseases and acute cerebral vascular diseases. This article will introduce the Japan Brain Science Society
{"title":"The pathogenesis and clinical features of cerebrovascular disease in diabetes mellitus","authors":"Jinlong Cheng, Bolin Chen","doi":"10.20821/JBS.45.0_45","DOIUrl":"https://doi.org/10.20821/JBS.45.0_45","url":null,"abstract":"45 Review The pathogenesis and clinical features of cerebrovascular disease in diabetes mellitus Jinlong Cheng1, Bolin Chen2,* 1. Department of Internal medicine , Tianjin MingJin metabolic disease hospital, Tianjin 300381,China 2. Department of Physiology and Pathophysiology, Tianjin Medical University Tianjin 300070, China * Correspondence to Bolin Chen E-mail: econversation@163.com Received:2015-02-01 Accepted:2015-03-01 Abstract Cerebrovascular disease is a kind of complications in diabetes mellitus which is induced by suger, fat and protein metabolic disorder. These series of nutrient metabolic disorder can lead to intracranial large blood vessels and microvascular lesions. About 20-40 percent of type 2 diabetes patients will suffer from cerebrovascular diseases which become the main causes of death in diabetic patients [1]. Recently many kinds of pathogenesis have been found by researchers about cerebrovascular diseases in diabetes mellitus such as hyperglycemia, insulin resistance [2], endothelial cell dysfunction [3], abnormal lipids metabolism and so on. The major clinical manifestations of diabetic cerebrovascular diseases are asymptomatic cerebral atherosclerosis, stroke, cerebral small vessel diseases and acute cerebral vascular diseases. This article will introduce the Japan Brain Science Society","PeriodicalId":15186,"journal":{"name":"Journal of Behavioral and Brain Science","volume":"24 1","pages":"45-56"},"PeriodicalIF":0.0,"publicationDate":"2015-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90699027","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
35 Research and Report To alleviate the mental stress of the hospital staff by the use of Morita therapy Yandong Wang1, Yan Wu2,Xuelong Jin3* 1. Tianjin Nankai hospital, Tianjin 300100, china 2. Nankai University, Tianjin 300071, China 3. Tianjin MingJin metabolic disease hospital, Tianjin 300381,China * Correspondence to Xuelong Jin E-mail: sentianxinli@163.com Received:2015-1-10 Accepted:2015-2-10
{"title":"To alleviate the mental stress of the hospital staff by the use of Morita therapy","authors":"Yandong Wang, Yan Wu, Xuelong Jin","doi":"10.20821/JBS.45.0_35","DOIUrl":"https://doi.org/10.20821/JBS.45.0_35","url":null,"abstract":"35 Research and Report To alleviate the mental stress of the hospital staff by the use of Morita therapy Yandong Wang1, Yan Wu2,Xuelong Jin3* 1. Tianjin Nankai hospital, Tianjin 300100, china 2. Nankai University, Tianjin 300071, China 3. Tianjin MingJin metabolic disease hospital, Tianjin 300381,China * Correspondence to Xuelong Jin E-mail: sentianxinli@163.com Received:2015-1-10 Accepted:2015-2-10","PeriodicalId":15186,"journal":{"name":"Journal of Behavioral and Brain Science","volume":"111 1","pages":"35-44"},"PeriodicalIF":0.0,"publicationDate":"2015-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73701453","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Radiation therapy, the most commonly used for the treatment of brain tumors, has been shown to be of major significance in tumor control and survival rate of brain tumor patients. About 200,000 patients with brain tumor are treated with either partial large field or whole brain radiation every year in China. The use of radiation therapy for treatment of brain tumors, however, may lead to devastating functional deficits in brain several months to years after treatment. An initial brain pathology resulting from exposure to radiation appears to be the dysfunction or disruption of the blood-brain barrier (BBB) and edema formation, which resulted from loss of tight junction (TJ) proteins and BBB components pericytes and astrocyte end-feet. Both of these scenarios lead to apoptosis of endothelial and neural cells and neuroinflammation in and around capillaries, which may progress into a variety of neurological impairments. It’s been found that Bone-marrow-derived EPCs (endothelial progenitor cells) play an integral role in the regulation and protection of the endothelium, as well as new vessel formation. It can incorporate into injured vessels and become mature endothelial cells during re-endothelialization and neovascularization processes, so the transplantation of EPCs into ischemic tissues provide a novel therapeutic option for radiation-induced brain injury. The efficacy of EPCs repairing disrupted BBB can be evaluated from the changes of expression of S100B, VEGF and EBA. is a non-invasive method that can be used to track labeled transplanted cells which can show the exact trace of EPCs in the region of brain injury. This review discusses the therapeutic potential radiation-induced brain injury.
{"title":"Endothelial Progenitor Cells : implications for radiation-induced brain injury","authors":"Q. Liu, Xuelong Jin","doi":"10.20821/JBS.44.0_42","DOIUrl":"https://doi.org/10.20821/JBS.44.0_42","url":null,"abstract":"Radiation therapy, the most commonly used for the treatment of brain tumors, has been shown to be of major significance in tumor control and survival rate of brain tumor patients. About 200,000 patients with brain tumor are treated with either partial large field or whole brain radiation every year in China. The use of radiation therapy for treatment of brain tumors, however, may lead to devastating functional deficits in brain several months to years after treatment. An initial brain pathology resulting from exposure to radiation appears to be the dysfunction or disruption of the blood-brain barrier (BBB) and edema formation, which resulted from loss of tight junction (TJ) proteins and BBB components pericytes and astrocyte end-feet. Both of these scenarios lead to apoptosis of endothelial and neural cells and neuroinflammation in and around capillaries, which may progress into a variety of neurological impairments. It’s been found that Bone-marrow-derived EPCs (endothelial progenitor cells) play an integral role in the regulation and protection of the endothelium, as well as new vessel formation. It can incorporate into injured vessels and become mature endothelial cells during re-endothelialization and neovascularization processes, so the transplantation of EPCs into ischemic tissues provide a novel therapeutic option for radiation-induced brain injury. The efficacy of EPCs repairing disrupted BBB can be evaluated from the changes of expression of S100B, VEGF and EBA. is a non-invasive method that can be used to track labeled transplanted cells which can show the exact trace of EPCs in the region of brain injury. This review discusses the therapeutic potential radiation-induced brain injury.","PeriodicalId":15186,"journal":{"name":"Journal of Behavioral and Brain Science","volume":"78 1","pages":"42-62"},"PeriodicalIF":0.0,"publicationDate":"2014-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88454511","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
M. Furuya, T. Miyaoka, S. Hashioka, R. Wake, K. Tsuchie, J. Horiguchi
Brain-derived neurotrophic factor (BDNF) is expressed at high levels in the hippocampal dentate gyrus (DG), and decreased levels of BDNF have been implicated in the pathophysiology of schizophrenia (SCZ). We have previously reported that yokukansan (YKS), which is a traditional Japanese medicine, is effective for SCZ and promotes neurogenesis in the DG of Gunn rats, an animal model of SCZ. In this study, we investigated the effect of YKS on serum BDNF levels in Gunn rats. The results showed that YKS increased serum BDNF in this model, which may suggest that BDNF expression in the DG leads to increased neurogenesis. Our findings may help to explain the efficacy of YKS in treating SCZ.
{"title":"Yokukansan increases serum Brain-derived neurotrophic factor (BDNF) levels in Gunn rat","authors":"M. Furuya, T. Miyaoka, S. Hashioka, R. Wake, K. Tsuchie, J. Horiguchi","doi":"10.20821/JBS.44.0_34","DOIUrl":"https://doi.org/10.20821/JBS.44.0_34","url":null,"abstract":"Brain-derived neurotrophic factor (BDNF) is expressed at high levels in the hippocampal dentate gyrus (DG), and decreased levels of BDNF have been implicated in the pathophysiology of schizophrenia (SCZ). We have previously reported that yokukansan (YKS), which is a traditional Japanese medicine, is effective for SCZ and promotes neurogenesis in the DG of Gunn rats, an animal model of SCZ. In this study, we investigated the effect of YKS on serum BDNF levels in Gunn rats. The results showed that YKS increased serum BDNF in this model, which may suggest that BDNF expression in the DG leads to increased neurogenesis. Our findings may help to explain the efficacy of YKS in treating SCZ.","PeriodicalId":15186,"journal":{"name":"Journal of Behavioral and Brain Science","volume":"20 1","pages":"34-41"},"PeriodicalIF":0.0,"publicationDate":"2014-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75382779","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}