• Title/Summary/Keyword: Brain Hippocampus

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Effect of whole Body Vibration Exercise on Intracerebral Hemorrhage in Rats (흰쥐 해마 CA1 부위의 뇌출혈 유발 시 전신진동운동의 효과)

  • Kim, Bo-Kyun;Yoon, Sung-Jin;Kim, Dong-Hyun;Ko, Il-Gyu;Kim, Chang-Ju;Jee, Yong-Seok;Shin, Mal-Soon
    • Korean Journal of Exercise Nutrition
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    • v.13 no.2
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    • pp.147-153
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    • 2009
  • Effect of whole body vibration exercise on intracerebral hemorrhage in rats. Intracerebral hemorrhage is one of the most devastating types of stroke. This disease is known to cause severe neurological damage and also has a very high mortality rate. In the present study, the effects of whole body vibration exercise on memory capability and apoptotic neuronal cell death in the hippocampal CA1 region following intracerebral hemorrhage in rats were investigated. Intracerebral hemorrhage was induced by injection of collagenase into the hippocampal CA1 region using a stereotaxic instrument. The rats were divided into 5 groups: the sham-operation group, the hemorrhage-induction group, the hemorrhage-induction and 8 Hz vibration exercise group, the hemorrhage-induction and 16 Hz vibration exercise group, and the hemorrhage-induction and 24 Hz vibration exercise group. The animals in the whole body vibration exercise groups received whole body vibration at 8 Hz, 16 Hz, and 24 Hz, respectively for 30 min once a day during 14 consecutive days. In the present results, the apoptotic neuronal cell death in the hippocampal CA1 region was significantly increased following induction of intracerebral hemorrhage, resulting in memory impairment. Whole body vibration exercise suppressed hemorrhage-induced apoptosis in the hippocampal CA1 region. This suppressive effect of whole body vibration exercise also alleviated hemorrhage-induced memory impairment. Here in this study, we have shown that whole body vibration exercise inhibited intracerebral hemorrhage-induced apoptotic neuronal cell death and thus facilitated recovery of brain function following intracerebral hemorrhage.

Raw Inonotus obliquus polysaccharide counteracts Alzheimer's disease in a transgenic mouse model by activating the ubiquitin-proteosome system

  • Shumin Wang;Kaiye Dong;Ji Zhang;Chaochao Chen;Hongyan Shuai;Xin Yu
    • Nutrition Research and Practice
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    • v.17 no.6
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    • pp.1128-1142
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    • 2023
  • BACKGROUND/OBJECTIVES: Inonotus obliquus has been used as antidiabetic herb around the world, especially in the Russian and Scandinavian countries. Diabetes is widely believed to be a key factor in Alzheimer's disease (AD), which is widely considered to be type III diabetes. To investigate whether I. obliquus can also ameliorate AD, it would be interesting to identify new clues for AD treatment. We tested the anti-AD effects of raw Inonotus obliquus polysaccharide (IOP) in a mouse model of AD (3×Tg-AD transgenic mice). MATERIALS/METHODS: SPF-grade 3×Tg-AD mice were randomly divided into three groups (Control, Metformin, and raw IOP groups, n = 5 per group). β-Amyloid deposition in the brain was analyzed using immunohistochemistry for AD characterization. Gene and protein expression of pertinent factors of the ubiquitin-proteasome system (UPS) was determined using real-time quantitative polymerase chain reaction and Western blotting. RESULTS: Raw IOP significantly reduced the accumulation of amyloid aggregates and facilitated UPS activity, resulting in a significant reduction in AD-related symptoms in an AD mouse model. The presence of raw IOP significantly enhanced the expression of ubiquitin, E1, and Parkin (E3) at both the mRNA and protein levels in the mouse hippocampus. The mRNA level of ubiquitin carboxyl-terminal hydrolase isozyme L1, a key factor involved in UPS activation, also increased by approximately 50%. CONCLUSIONS: Raw IOP could contribute to AD amelioration via the UPS pathway, which could be considered as a new potential strategy for AD treatment, although we could not exclude other mechanisms involved in counteracting AD processing.

LP-M, a Novel Butanol-Extracts Isolated from Liriope platyphylla, could Induce the Neuronal Cell Survival and Neuritic Outgrowth in Hippocampus of Mice through Akt/ERK Activation on NGF Signal Pathway (맥문동(Liriope platyphylla)의 새로운 부탄올 추출물인 LP-M이 Akt/ERK NGF receptor signaling pathway를 통해 뇌조직에서 신경세포의 생존과 성장에 미치는 영향에 관한 연구)

  • Nam, So-He;Choi, Sun-Il;Goo, Jun-Seo;Kim, Ji-Eun;Lee, Yoen-Kyung;Hwang, In-Sik;Lee, Hye-Ryun;Lee, Young-Ju;Lee, Hong-Gu;Choi, Young-Whan;Hwang, Dae-Youn
    • Journal of Life Science
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    • v.21 no.9
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    • pp.1234-1243
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    • 2011
  • Liriope platyphylla has been used in oriental medicine as an effective medical plant to improve symptoms of cough, sputum production, neurodegenerative disorders, obesity and diabetes for long time. In order to investigate the effects of novel extracts on nerve growth factors (NGF)-stimulated neuritic outgrowth, the alteration of NGF expression and NGF receptor signaling pathway were detected in neuroblastoma cells and C57BL/6 mice. Of a total of 13 novel extracts, 4 extracts (LP-E, LP-M, LP-M50, LP2E17PJ) showed high viability on MTT assay. Also, all of these extracts induced NGF secretion and NGF mRNA expression in neuroblastoma cells. However, the NGF-induced neuritic outgrowth from PC12 cells was only stimulated by LP-E, LP-M and LP-M50. Furthermore, we selected LP-M as a best candidate, based on method and amounts of extraction, in order to verify its effect in mice. C57BL/6 mice were treated with 50 mg/kg of LP-M for 2 weeks and the effects on NGF regulation were analyzed with various methods. The expression of NGF mRNA was significantly increased in LP-M treated mice compared to vehicle treated mice. Also, the signaling pathway of p75NTR was inhibited in the cortex by LP-M treatment, with no change in the hippocampus of brain. However, the signaling pathway of TrkA was dramatically activated in only hippocampus via LP-M treatment. Therefore, these results suggest that the novel four extracts of L. platyphylla may contribute to the regulation of NGF expression and secretion in neuronal cells. LP-M was especially considered to be an excellent candidate for a neurodegenerative disease-therapeutic drug.

Effects of tianeptine on symptoms of fibromyalgia via BDNF signaling in a fibromyalgia animal model

  • Lee, Hwayoung;Im, Jiyun;Won, Hansol;Nam, Wooyoung;Kim, Young Ock;Lee, Sang Won;Lee, Sanghyun;Cho, Ik-Hyun;Kim, Hyung-Ki;Kwon, Jun-Tack;Kim, Hak-Jae
    • The Korean Journal of Physiology and Pharmacology
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    • v.21 no.4
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    • pp.361-370
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    • 2017
  • Previous reports have suggested that physical and psychological stresses may trigger fibromyalgia (FM). Stress is an important risk factor in the development of depression and memory impairments. Antidepressants have been used to prevent stress-induced abnormal pain sensation. Among various antidepressants, tianeptine has been reported to be able to prevent neurodegeneration due to chronic stress and reverse decreases in hippocampal volume. To assess the possible effect of tianeptine on FM symptoms, we constructed a FM animal model induced by restraint stress with intermittent cold stress. All mice underwent nociceptive assays using electronic von Frey anesthesiometer and Hargreaves equipment. To assess the relationship between tianeptine and expression levels of brain-derived neurotrophic factor (BDNF), cAMP response element-binding protein (CREB), and phosphorylated cAMP response element-binding protein (p-CREB), western blotting and immunohistochemistry analyses were performed. In behavioral analysis, nociception tests showed that pain threshold was significantly decreased in the FM group compared to that in the control group. Western blot and immunohistochemical analyses of medial prefrontal cortex (mPFC) and hippocampus showed downregulation of BDNF and p-CREB proteins in the FM group compared to the control group. However, tianeptine recovered these changes in behavioral tests and protein level. Therefore, this FM animal model might be useful for investigating mechanisms linking BDNF-CREB pathway and pain. Our results suggest that tianeptine might potentially have therapeutic efficacy for FM.

The Neuroprotective Effect of White Ginseng (Panax ginseng C. A. Meyer) on the Trimethyltin (TMT)-Induced Memory Deficit Rats (Trimethyltin으로 유도된 기억장애 흰쥐에서 백삼의 신경보호효과)

  • Lee, Seung-Eun;Shim, In-Sop;Kim, Geum-Soog;Yim, Sung-Vin;Park, Hyun-Jung;Shim, Hyun-Soo;Ye, Min-Sook;Kim, Seung-Yu
    • Korean Journal of Medicinal Crop Science
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    • v.19 no.6
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    • pp.456-463
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    • 2011
  • The present study examined the effects of Korean white ginseng (WG, Panax ginseng C. A. Meyer) on the learning and memory function and the neural activity in rats with trimethyltin (TMT)-induced memory deficits. The rats were administered with saline or WG (WG 100 or 300 mg/kg, p.o.) daily for 21 days. The cognitive improving efficacy of WG on the amnesic rats, which was induced by TMT, was investigated by assessing the Morris water maze test and by performing immunohistochemistries on choline acetyltransferase (ChAT), acetylcholinesterase (AchE), cAMP responsive element binding protein (CREB) and brain derived neurotrophic factor (BDNF). The rats treated with TMT injection (control group) showed impaired learning and memory of the tasks, but the rats treated with TMT injection and WG administration produced significant improvement of the escape latency to find the platform in the Morris water maze at the 2nd and 4th days compared to that of the control group. In the retention test, the WG 100 and WG 300 groups showed significantly increased crossing number around the platform compared to that of the control group (p < 0.001). Consistently with the behavioral data, result of immunohistochemistry analysis showed that WG 100 mg/kg significantly alleviated the loss of BDNF-ir neurons in the hippocampus compared to that of the control group (p < 0.01). Also, treatment with WG has a trend to be increased the cholinergic neurons in the hippocampal CA1 and CA3 areas as compared to that of the control group. These results suggest that WG may be useful for improving the cognitive function via regulation of neurotrophic activity.

Neuro-inflammation induced by restraint stress causes impairs neurobehavior in mice (스트레스 유발 마우스모델에서 뇌염증 및 신경행동 장애 변화)

  • Oh, Tae woo;Do, Hyun Ju;Kim, Kwang-Youn;Kim, Young Woo;Lee, Byung Wook;Ma, Jin Yeul;Park, Kwang Il
    • Herbal Formula Science
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    • v.25 no.4
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    • pp.483-497
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    • 2017
  • Background : Behavioral stress has been suggested as one of the significant factors that is able to disrupt physiological systems and cause depression as well as changes in various body systems. The stressful events can alter cognition, learning, memory and emotional responses, resulting in mental disorders such as depression and anxiety. Results : We used a restraint stress model to evaluate the alteration of behavior and stress-related blood parameter. The animals were randomly divided into two groups of five animals each group. Furthermore, we assessed the change of body weight to evaluate the locomotor activity as well as status of emotional and anxiety in mice. After 7 days of restraint stress, the body weight had significantly decreased in the restraint stress group compared with the control group. We also observed stress-associated behavioral alterations, as there was a significant decrease in open field and forced swim test, whereas the immobilization time was significantly increased in the stress group compared to the control group. We observed the morphological changes of neuronal death and microglia by immunohistochemistry and western blot. In our study restraint stress did not cause change in neuronal cell density in the frontal cortex and CA1 hippocampus region, but there was a trend for an increased COX-2 and iNOS protein expression and microglia (CD11b) in brain, which is restraint stress. Conclusion : Our study, there were significant alterations observed in the behavioral studies. We found that mice undergoing restraint stress changed behavior, confirming the increased expression of inflammatory factors in the brain.

Beyond Clot Dissolution; Role of Tissue Plasminogen Activator in Central Nervous System

  • Kim, Ji-Woon;Lee, Soon-Young;Joo, So-Hyun;Song, Mi-Ryoung;Shin, Chan-Young
    • Biomolecules & Therapeutics
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    • v.15 no.1
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    • pp.16-26
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    • 2007
  • Tissue plasminogen activator (tPA) is a serine protease catalyzing the proteolytic conversion of plasminogen into plasmin, which is involved in thrombolysis. During last two decades, the role of tPA in brain physiology and pathology has been extensively investigated. tPA is expressed in brain regions such as cortex, hippocampus, amygdala and cerebellum, and major neural cell types such as neuron, astrocyte, microglia and endothelial cells express tPA in basal status. After strong neural stimulation such as seizure, tPA behaves as an immediate early gene increasing the expression level within an hour. Neural activity and/or postsynaptic stimulation increased the release of tPA from axonal terminal and presumably from dendritic compartment. Neuronal tPA regulates plastic changes in neuronal function and structure mediating key neurologic processes such as visual cortex plasticity, seizure spreading, cerebellar motor learning, long term potentiation and addictive or withdrawal behavior after morphine discontinuance. In addition to these physiological roles, tPA mediates excitotoxicity leading to the neurodegeneration in several pathological conditions including ischemic stroke. Increasing amount of evidence also suggest the role of tPA in neurodegenerative diseases such as Alzheimer's disease and multiple sclerosis even though beneficial effects was also reported in case of Alzheimer's disease based on the observation of tPA-induced degradation of $A{\beta}$ aggregates. Target proteins of tPA action include extracellular matrix protein laminin, proteoglycans and NMDA receptor. In addition, several receptors (or binding partners) for tPA has been reported such as low-density lipoprotein receptor-related protein (LRP) and annexin II, even though intracellular signaling mechanism underlying tPA action is not clear yet. Interestingly, the action of tPA comprises both proteolytic and non-proteolytic mechanism. In case of microglial activation, tPA showed non-proteolytic cytokine-like function. The search for exact target proteins and receptor molecules for tPA along with the identification of the mechanism regulating tPA expression and release in the nervous system will enable us to better understand several key neurological processes like teaming and memory as well as to obtain therapeutic tools against neurodegenerative diseases.

Fermented Saccharina japonica (Phaeophyta) improves neuritogenic activity and TMT-induced cognitive deficits in rats

  • Park, Hyun-Jung;Lee, Mi-Sook;Shim, Hyun Soo;Lee, Gyeong-Ran;Chung, Sun Yong;Kang, Young Mi;Lee, Bae-Jin;Seo, Yong Bae;Kim, Kyung Soo;Shim, Insop
    • ALGAE
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    • v.31 no.1
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    • pp.73-84
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    • 2016
  • Marine organisms are frequently used to be harmful and have lower side effects than synthetic drugs. The cognitive improving efficacy of gamma aminobutyric acid-enriched fermented Saccharina japonica (FSJ) on the memory deficient rats, which were induced by trimethyltin chloride (TMT), was investigated by assessing the Morris water maze test and by performing choline acetyltransferase (ChAT), cAMP response element binding protein (CREB), and brain derived neurotrophic factor (BDNF) immunohistochemistry. The neurite outgrowth of Neuro2a cells was assessed in order to examine the underlying mechanisms of the memory enhancing effects of FSJ. Treatment with FSJ tended to shorten the latency to find the platform in the acquisition test of the Morris water maze at the second and fourth day compared to the control group. In the probe trial, the FSJ treated group increased time spent in the target quadrant, compared to that of the control group. Consistent with the behavioral data, these treatments recovered the loss of ChAT, CREB, and BDNF immunepositive neurons in the hippocampus produced by TMT. Treatment with FSJ markedly stimulated neurite outgrowth of the Neuro2a cells as compared to that of the controls. These findings demonstrate that FSJ may be useful for improving the cognitive function via regulation of neurotrophic marker enzyme activity.

Neuroprotective Effect of Hwangryunhaedok-tang on the Brain Ischemia Induced by Four-Vessel Occlusion in Rats (황련해독탕(黃連解毒湯)의 4-VO로 유발한 흰쥐뇌허혈에 대한 신경보호효과)

  • 이민정;김영옥;이강진;유영법;김선여;김성수;김호철
    • The Journal of Korean Medicine
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    • v.23 no.4
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    • pp.161-168
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    • 2002
  • Objectives: Hwangryunhaedok-tang (Huang-lian-jie-du-tang, HRHDT, 黃連解毒湯) is a traditional Korean herbal medicine that is formulated with Coptidis Rhizoma, Phellodendri Cortex, Scutellariae Radix and Gardeniae Fructus. HRHDT is cold (寒) and bitter (苦) in nature and has general properties of clearing heat and detoxifying (淸熱解毒), strengthening the stomach and settling the liver (健胃平肝), and reducing inflammation, fever and swelling. This formula can prevent and treat artherosclerosis, hyperplasia of the endothelium, cerebral fluid circulation, cerebral vascular deterioration through aging, impairment of neurotransmitters, or disruption of the functioning of the cerebral cortex following infection or trauma. The purpose of the study reported here was to determine the neuroprotective effect of HRHDT on global ischemia induced by 4-vessel occlusion in Wistar rats. Methods: HRHDT extract was lyophilized after extraction with 85% methanol and 100% water. Rats were induced to 10 minutes of forebrain ischemia by 4-vessel occlusion (4-VO) and reperfused again. HRHDT was administered with a dose of 100 mg/kg, and 500 mg/kg of 85% methanol extracts and 100 mg/kg of 100% water extracts, respectively, at 0 min and 90 min after 4-VO. Rats were killed at 7 days after ischemia and the number of CA1 pyramidal neurons was counted in hippocampal sections stained with cresyl violet. Results: Body temperature of animals showed no significant difference between saline-treated groups and HRHDT extracts-treated groups until 5 hours of reperfusion. This result indicated that neuroprotective effects of HRHDT extracts were not due to hypothermic effects. The administration of HRHDT showed a significant neuroprotective effect on hippocampal CA1 neurons at 7 days after ischemia compared to the saline-treated group (P<0.001). HRHDT methanol extracts of 100 mg/kg, 500 mg/kg and HRHDT water extracts of 100 mg/kg showed 88.5%, 98.3% and 95.1 % neuroprotection, respectively. Conclusions: The results of this study demonstrate that administration of HRHDT is highly effective in reducing neuronal damage in response to transient global cerebral ischemia. HRHDT may involve many mechanisms that might account for its high degree of efficacy. A number of factors including free radicals, glutamate, calcium overload, NO, and various cytokines have been proposed to have an important role in causing neuronal death after short periods of global ischemia. Further studies are needed to know the neuroprotective mechanisms of HRHDT.

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A Study on the RFID Biometrics System Based on Hippocampal Learning Algorithm Using NMF and LDA Mixture Feature Extraction (NMF와 LDA 혼합 특징추출을 이용한 해마 학습기반 RFID 생체 인증 시스템에 관한 연구)

  • Oh Sun-Moon;Kang Dae-Seong
    • Journal of the Institute of Electronics Engineers of Korea SP
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    • v.43 no.4 s.310
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    • pp.46-54
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    • 2006
  • Recently, the important of a personal identification is increasing according to expansion using each on-line commercial transaction and personal ID-card. Although a personal ID-card embedded RFID(Radio Frequency Identification) tag is gradually increased, the way for a person's identification is deficiency. So we need automatic methods. Because RFID tag is vary small storage capacity of memory, it needs effective feature extraction method to store personal biometrics information. We need new recognition method to compare each feature. In this paper, we studied the face verification system using Hippocampal neuron modeling algorithm which can remodel the hippocampal neuron as a principle of a man's brain in engineering, then it can learn the feature vector of the face images very fast. and construct the optimized feature each image. The system is composed of two parts mainly. One is feature extraction using NMF(Non-negative Matrix Factorization) and LDA(Linear Discriminants Analysis) mixture algorithm and the other is hippocampal neuron modeling and recognition simulation experiments confirm the each recognition rate, that are face changes, pose changes and low-level quality image. The results of experiments, we can compare a feature extraction and learning method proposed in this paper of any other methods, and we can confirm that the proposed method is superior to the existing method.