Elucidating the Role of Brain-Derived Neurotrophic Factor in the Brain
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Neocortex
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Neurotrophin-3
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Objective To investigate the mechanism of Moxibustion pretreatment in prevention and cure of Alzheimer′s disease(AD).Methods Rats were randomly divided into normal,sham,model and moxibustion pretreatment groups(n=10).AD rats were induced by injecting β-amyloid25~35(Aβ25~35) into the double hippocampus.Bǎihui,Shenshū and Zusānlǐ acupoints were used to prevent and cure AD by moxibustion.Brain-derived neurotrophic factor(BDNF) and its receptor TrkB in hippocampus CA1 zone of rats were detected by immunohistochemistry.Results Compared with normal and sham group,the expression of BDNF and its receptor TrkB in model group were significantly decreased(P0.01).Compared with the model group,the expressions of BDNF and TrkB in moxibustion pretreatment group were significantly increased(P0.01).Conclusions Moxibustion pretreatment could effectively increase the expressions of BDNF and TrkB in hippocampus CA1 zone,ameliorate the neuron injury of the brain and protect the brain cells.
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Neocortex
Temporal cortex
Synaptogenesis
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Trk receptor
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Abstract The diffusible factors, nitric oxide (NO) and brain‐derived neurotrophic factor (BDNF) are both suggested to be intercellular messengers that have similar synaptic activities and developmental influences in the brain. In the present study, we have analysed their mutual regulation with respect to their production in rodent neocortical neurons. Some of the cultured rat neocortical neurons exhibited immunoreactivity for both neuronal NO synthase (NOS) and the BDNF receptor trkB. Neuronal NOS appeared to be activated autonomously and produced NO in culture as monitored by nitrite accumulation. Inhibition of the endogenous NO production in culture by a NOS inhibitor, N G ‐monomethyl‐ l ‐arginine (NMMA), enhanced basal expression of BDNF mRNA and protein. Similarly, cerebroventricular administration of another NOS inhibitor, N‐ω‐nitro‐ l ‐arginine methylester ( l ‐NAME), but not d ‐NAME or saline, increased BDNF content in the neocortex. In the opposite direction, however, BDNF appeared to function as a positive regulator for NO synthesis. Addition of BDNF upregulated the neuronal NOS expression as well as NO production in neocortical culture. In agreement, BDNF knock‐out mice exhibited significant impairment of neuronal NOS expression in the neocortex. Taken together, these observations suggest that the trans‐synaptic signalling molecules, NO and BDNF, influence the production of each other and mutually regulate the strength of their intercellular communications.
Neocortex
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ABSTRACT In certain neurons, zinc ions are stored in synaptic vesicles by zinc transporter 3 (ZnT3). Vesicular zinc can then be released synaptically to modulate myriad targets. In vitro evidence indicates that these targets may include brain-derived neurotrophic factor (BDNF) and its receptor, tropomyosin receptor kinase B (TrkB). But the effects of vesicular zinc on BDNF and TrkB in the intact brain are unclear. Studies of mice that lack ZnT3 – and, as a result, vesicular zinc – have shown abnormalities in BDNF and TrkB levels, but results have been mixed and are therefore difficult to interpret. This might be caused by differences in the age or sex of mice tested. In the present study, we measured BDNF and TrkB levels in the hippocampus and neocortex, comparing wild type and ZnT3 knockout mice of both sexes at two ages (5 and 12 weeks). We also examined BDNF mRNA expression and protein levels at an intermediate age (8-10 weeks). We found that, regardless of age or sex, BDNF and TrkB protein levels did not differ between wild type and ZnT3 knockout mice. There were sex-specific differences in BDNF protein and mRNA expression, however. BDNF protein levels increased with age in female mice but not in males. And in females, but not males, ZnT3 KO mice exhibited great hippocampal BDNF mRNA expression than wild type mice. We conclude that, at least in naïve mice housed under standard laboratory conditions, elimination of vesicular zinc does not affect BDNF or TrkB protein levels.
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Neocortex
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Astrocytes are emerging in the neuroscience field as crucial modulators of brain functions, from the molecular control of synaptic plasticity to orchestrating brain-wide circuit activity for cognitive processes. The cellular pathways through which astrocytes modulate neuronal activity and plasticity are quite diverse. In this review, we focus on neurotrophic pathways, mostly those mediated by brain-derived neurotrophic factor (BDNF). Neurotrophins are a well-known family of trophic factors with pleiotropic functions in neuronal survival, maturation and activity. Within the brain, BDNF is the most abundantly expressed and most studied of all neurotrophins. While we have detailed knowledge of the effect of BDNF on neurons, much less is known about its physiology on astroglia. However, over the last years new findings emerged demonstrating that astrocytes take an active part into BDNF physiology. In this work, we discuss the state-of-the-art knowledge about astrocytes and BDNF. Indeed, astrocytes sense extracellular BDNF through its specific TrkB receptors and activate intracellular responses that greatly vary depending on the brain area, stage of development and receptors expressed. Astrocytes also uptake and recycle BDNF / proBDNF at synapses contributing to synaptic plasticity. Finally, experimental evidence is now available describing deficits in astrocytic BDNF in several neuropathologies, suggesting that astrocytic BDNF may represent a promising target for clinical translation.
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Objective To observe the effect of chronic unpredicted sequence of mild stress(CUMS)and fluoxetine on the expression of brain-derived neurotrophic factor(BDNF),neurotrophin-3(NT-3)and their functional receptors TrkB/trkC in the hippocampus and Amygdoid nuclei of adult rat.Methods Thirty-two male SD rats were randomly and equally allocated to 4 groups.Quantative reverse transcription polymerase chain reaction(RT-PCR)and immunohistochemistry were used to examine the expression levels of BDNF/TrkB and NT-3/TrkC protein and mRNA after CUMS and fluoxetine management.Results After the experiment,the opposite regulation of BDNF in the hippocampus and similar in the Amygdoid nuclei were shown to compare with their control groups,different expression direction of NT-3 in the hippocampus and Amygdoid nuclei was presented.And changes in the pattern of their receptors TrkB/trkC differed from their corresponding ligand.Conclusion Different models of expression in CUMS and fluoxetine groups suggested a role for them in the onset of antidepressive effectivity and the pathogenesis of depression.
Neurotrophin-3
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