[Electroacupuncture Stimulation of Different Acupoint or Paired Acupoints on Expression of BDNF and TrkB Proteins and Genes in Hippocampus in Myocardial Ischemic Rats].
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To observe the protective effect of electroacupuncture (EA) intervention on the expression of brain-derived-neurotrophic factor (BDNF) and tropomyosin receptor kinase B (TrkB) proteins and genes in the hippocampus areas in myocardial ischemia (MI) rats, so as to reveal its underlying mechanisms in protecting hippocampal cells under MI.Eighty healthy male SD rats were randomized into sham-operation (sham), MI model, Shenmen (HT 7), HT 7-Zhizheng (SI 7) and HT 7-Xinshu (BL 15) groups (n = 15 in each group). The MI model was established by occlusion of the anterior descending branch of the left coronary artery. EA (2 Hz, 2 mA) was applied to bilateral HT 7, HT 7-SI 7, and HT 7-BL 15, respectively for 15 min, once per day for a week. The number of BDNF and its receptor TrkB positive cells in the left hippocampus and that of mRNAs in the right hippocampus tissue were determined by immunohistochemistry and real-time fluorescence quantitative PCR, respectively.In comparison with the sham group, the numbers of both BDNF and TrkB positive cells in the left hippocampus and the expression levels of BDNF mRNA and TrkB mRNA in the right hippocampus were increased slightly (P > 0.05). After EA intervention, the numbers of hippocampal BDNF and TrkB positive cells and the expression levels of BDNF mRNA and TrkB mRNA were evidently up-regulated (P < 0.05, P < 0.01), and the effects of HT 7-SI 7 and HT 7-BL 15 were obviously superior to those of simple HT 7 in up-regulating BDNF and TrkB expression (P < 0.01, P < 0.05). No significant differences were found between the HT 7-SI 7 and HT 7-BL 15 groups in increasing the number of hippocampal BDNF and TrkB positive cells and in up-regulating expression of both BDNF mRNA and TrkB mRNA (P > 0.05).EA intervention is effective in increasing the expression of hippocampal BDNF and TrkB in MI rats, which may contribute to its effect in protecting hippocampal cells from injury under MI condition. The effect of EA stimulation of HT 7-SI 7 and HT 7-BL 15 was obviously superior to that of simple HT 7 in up-regulating BDNF and TrkB expression.Cite
Objective:To investigate the influence of electroacupuncture therapy on the expession of neurotrophic factor and their receptors,explore the mechanism of electroacupuncture in treatment of Alzheimer's disease.Methods: Forty Wistar rats were randomly divided into 4 groups:a normal group,a sham-operation group,a model group and a electroacupuncture group.AD rats were induced by injecting β-Amyloid 25-35(Aβ25-35) into the double hippocampus.Fengfu point was acupunctured in electroacupuncture group,A behavioral examination was made by Morris Water-Maze.Immunohistochemistry was used to detect the expression of thehippocampus BDNF、TrkB、GDNF and GFR-α1.Results:The number of BDNF、TrkB、GDNF and GFR-α1 postive cells in hippocampus of model group were significantly lower than that of normal group(P0.05),the number of BDNF、TrkB、GDNF and GFR-α1 postive cells in hippocampus of electroacupuncture group were significantly higher than that of model group(P0.01).Conclusion: Electroacupuncture therapy in Fengfu point can increase the expression of BDNF、TrkB、GDNF and GFR-α1 in hippocampus of the Alzheimerian rats,and protect cholinergic neurons from injure.
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To observe the protective effect of electroacupuncture (EA) intervention on the expression of brain-derived-neurotrophic factor (BDNF) and tropomyosin receptor kinase B (TrkB) proteins and genes in the hippocampus areas in myocardial ischemia (MI) rats, so as to reveal its underlying mechanisms in protecting hippocampal cells under MI.Eighty healthy male SD rats were randomized into sham-operation (sham), MI model, Shenmen (HT 7), HT 7-Zhizheng (SI 7) and HT 7-Xinshu (BL 15) groups (n = 15 in each group). The MI model was established by occlusion of the anterior descending branch of the left coronary artery. EA (2 Hz, 2 mA) was applied to bilateral HT 7, HT 7-SI 7, and HT 7-BL 15, respectively for 15 min, once per day for a week. The number of BDNF and its receptor TrkB positive cells in the left hippocampus and that of mRNAs in the right hippocampus tissue were determined by immunohistochemistry and real-time fluorescence quantitative PCR, respectively.In comparison with the sham group, the numbers of both BDNF and TrkB positive cells in the left hippocampus and the expression levels of BDNF mRNA and TrkB mRNA in the right hippocampus were increased slightly (P > 0.05). After EA intervention, the numbers of hippocampal BDNF and TrkB positive cells and the expression levels of BDNF mRNA and TrkB mRNA were evidently up-regulated (P < 0.05, P < 0.01), and the effects of HT 7-SI 7 and HT 7-BL 15 were obviously superior to those of simple HT 7 in up-regulating BDNF and TrkB expression (P < 0.01, P < 0.05). No significant differences were found between the HT 7-SI 7 and HT 7-BL 15 groups in increasing the number of hippocampal BDNF and TrkB positive cells and in up-regulating expression of both BDNF mRNA and TrkB mRNA (P > 0.05).EA intervention is effective in increasing the expression of hippocampal BDNF and TrkB in MI rats, which may contribute to its effect in protecting hippocampal cells from injury under MI condition. The effect of EA stimulation of HT 7-SI 7 and HT 7-BL 15 was obviously superior to that of simple HT 7 in up-regulating BDNF and TrkB expression.
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Aim: Brain‐derived neurotrophic factor (BDNF) reduces plasma glucose levels in obese db/db diabetic mice and is speculated to produce its effects via the hypothalamus, the regulatory centre of satiety and the autonomic nervous system. The potential effect of BDNF directly on peripheral endocrine organs, however, remains to be clarified. Here we report the effects of BDNF on hormonal secretion from pancreatic islets of Langerhans using their isolated culture. Methods and results: In an immunohistochemical study, mouse pancreatic alpha cells were stained specifically with the anti‐TrkB (a specific receptor for BDNF) antibody. After 7 days culture of isolated islets of the normal mouse pancreas, 10 ng/ml BDNF decreased the secretion of glucagon per 6 h significantly less than that of the control (p = 0.016). In contrast, there were no significant changes in insulin secretion or glucagon and insulin contents in the islets cultured under the same conditions. In vivo administration of BDNF (10 mg/kg/day) to normal mice for 7 days significantly decreased their food consumption (p < 0.05). The fasting plasma glucose levels were decreased on day 7 compared with day 1 more significantly in BDNF‐treated mice (p = 0.043) than in pair‐fed control mice (p = 0.14). In newborn BDNF‐knockout mice, fasting plasma glucose levels increased in the order of homozygote, heterozygote and wild type (p = 0.033). No apparent immunohistochemical abnormality was observed for pancreatic glucagon in the BDNF‐knockout mice. Conclusion: These data suggest that BDNF affects glucose metabolism not only with its anorectic effect but also with modulated glucagon secretion from pancreatic alpha cells.
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Enteroendocrine cell
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Abstract The hippocampus plays a key role in learning and emotional regulation. The hippocampus’ function varies along its septotemporal axis, with the septal pole being more frequently involved in spatial learning and memory, and the temporal pole playing a greater role in emotional behaviors. In this study, we present findings aimed at checking the expression level of the genes encoding neurotrophins and their receptors, including nerve growth factor ( NGF ), brain‐derived neurotrophic factor ( BDNF ), neurotrophin‐3 ( NT ‐3), and their receptors ( TrkA , TrkB and TrkC ) in the hippocampus along the septotemporal axis. Using real‐time PCR , several different expression patterns were observed. Remarkably, the expression of both NT ‐3 and TrkA genes in the septal hippocampus was higher than in the middle and temporal hippocampus. Higher expression of NT ‐3 and TrkA may implicate active neurogenesis in the dentate gyrus ( DG ) of the septal hippocampus because more neurogenesis occurs in the septal than the temporal DG of rats. Finally, the results obtained in this study emphasize the importance of choosing the hippocampal portion along its septotemporal axis for any hippocampal molecular and biochemical experimental studies.
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Depression
Chronic Stress
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Post-Stroke Depression
Stroke
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Water maze
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Running is a potent stimulator of cell proliferation in the adult dentate gyrus and these newly generated hippocampal neurons seem to be implicated in memory functions. Here we have used a mouse model expressing activated Ras under the direction of the neuronal Synapsin I promoter (named synRas mice). These mice develop down-regulated proliferation of adult hippocampal precursor cells and show decreased short-term recognition memory performances. Voluntary physical activity reversed the genetically blocked generation of hippocampal proliferating cells and enhanced the dendritic arborisation of the resulting doublecortin newly generated neurons. Moreover, running improved novelty recognition in both wild type and synRas littermates, compensating their memory deficits. Brain-derived neurotrophic factor (BDNF) has been proposed to be a potential mediator of physical exercise acting in the hippocampus on dentate neurons and their precursors. This was confirmed here by the identification of doublecortin-immunoreactive cells expressing tyrosine receptor kinase B BDNF receptor. While no difference in BDNF levels were detected in basal conditions between the synRas mice and their wild type littermates, running was associated with enhanced BDNF expression levels. Thus increased BDNF signalling is a candidate mechanism to explain the observed effects of running. Our studies demonstrate that voluntary physical activity has a robust beneficial effect even in mice with genetically restricted neurogenesis and cognition.
Doublecortin
Synapsin I
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Objective To evaluate the effects of electroacupuncture (EA) at the Baihui (DU 20) and Dazhui (Bill) points on brain derived neurotrophic factor (BDNF) around the area of cerebral infarction and evaluate the relation between learning and memory ability and BDNF. Methods Forty-eight male adult Wistar rats were divided randomly and equally into EA and control groups. The EA group was sub-divided into 1 week, 2 weeks and 3weeks sub-groups. EA was started 24 h after establishing a model of ischemic brain injury and continued for one, two or three weeks. The control group was reared conventionally and was not given any treatment. Morris' water maze test was used to evaluate the rats' learning and memory ability. The expression of BDNF in the CA3 region of the hippo campus was detected using immunohistochemical techniques. Results Learning and memory in the EA groups were better than in the control group, and spatial probe ability was also significantly better. Positive expression of BDNF was detected in the hippocampal CA3 region of the EA group rats, and it was significantly greater than that in the control group. Conclusion Learning and memory after cerebral infarction can be affected by EA at the Baihui and Dazhui points. The effect might be related with increased BDNF expression in the hippocampal CA3 region.
Key words:
Cerebral ischemia; Learning; Memory; Electroacupuncture; Neurotrophic factors; Rats
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