Antidepressant Drugs Correct the Imbalance Between proBDNF/p75NTR/Sortilin and Mature BDNF/TrkB in the Brain of Mice with Chronic Stress

Yang, Chunrui; Y., Zhang, X.; Liu, Y.; Du, Jenny; Liang, Ruixing; Yu, Mei; Zhang, F. Q.; Mu, Xiaofeng; Li, F.; Zhou, Li; Zhou, Fiona H.; Meng, Fanjie; Wang, S.; Ming, Dong; Zhou, Xin

doi:10.1007/s12640-019-00101-2

Cited by 34 publications

(26 citation statements)

References 39 publications

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“…miRNAs could be an effective target also for the treatment of depression. Recent data demonstrate that miR-124-mediated post-transcriptional regulation of CREB1 and BDNF can improve depression-like behavior in a rat model [ 61 ]. Instead, miR-153 through the inhibition of activation of the JAK-STAT signaling pathway improves BDNF expression and influences the proliferative ability of hippocampal neurons in autistic mice [ 62 ].…”

Section: The Human Bdnf Gene: Transcripts and Variantsmentioning

confidence: 99%

Neurotrophic Factor BDNF, Physiological Functions and Therapeutic Potential in Depression, Neurodegeneration and Brain Cancer

Colucci-D’Amato

Speranza

Volpicelli

2020

IJMS

386

202

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Brain-derived neurotrophic factor (BDNF) is one of the most distributed and extensively studied neurotrophins in the mammalian brain. BDNF signals through the tropomycin receptor kinase B (TrkB) and the low affinity p75 neurotrophin receptor (p75NTR). BDNF plays an important role in proper growth, development, and plasticity of glutamatergic and GABAergic synapses and through modulation of neuronal differentiation, it influences serotonergic and dopaminergic neurotransmission. BDNF acts as paracrine and autocrine factor, on both pre-synaptic and post-synaptic target sites. It is crucial in the transformation of synaptic activity into long-term synaptic memories. BDNF is considered an instructive mediator of functional and structural plasticity in the central nervous system (CNS), influencing dendritic spines and, at least in the hippocampus, the adult neurogenesis. Changes in the rate of adult neurogenesis and in spine density can influence several forms of learning and memory and can contribute to depression-like behaviors. The possible roles of BDNF in neuronal plasticity highlighted in this review focus on the effect of antidepressant therapies on BDNF-mediated plasticity. Moreover, we will review data that illustrate the role of BDNF as a potent protective factor that is able to confer protection against neurodegeneration, in particular in Alzheimer’s disease. Finally, we will give evidence of how the involvement of BDNF in the pathogenesis of brain glioblastoma has emerged, thus opening new avenues for the treatment of this deadly cancer.

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Section: The Human Bdnf Gene: Transcripts and Variantsmentioning

confidence: 99%

Neurotrophic Factor BDNF, Physiological Functions and Therapeutic Potential in Depression, Neurodegeneration and Brain Cancer

Colucci-D’Amato

Speranza

Volpicelli

2020

IJMS

386

202

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“…The imbalance of the pro- and mature forms of BDNF has been observed in depressed patients and in rodent models of depression [ 299 , 300 , 301 ]. Furthermore, antidepressants were shown to correct this imbalance in the brain of chronically stressed mice [ 302 ]. GCs could further directly interrupt BDNF signaling, by inhibiting the prosurvival (PI3K/Akt; PLCγ) and proliferative (MAP kinase) pathways.…”

Section: Mechanisms Of Stress Acting On Neurogenesismentioning

confidence: 99%

Stress-Related Dysfunction of Adult Hippocampal Neurogenesis—An Attempt for Understanding Resilience?

Leschik

Lutz

Gentile

2021

IJMS

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Newborn neurons in the adult hippocampus are regulated by many intrinsic and extrinsic cues. It is well accepted that elevated glucocorticoid levels lead to downregulation of adult neurogenesis, which this review discusses as one reason why psychiatric diseases, such as major depression, develop after long-term stress exposure. In reverse, adult neurogenesis has been suggested to protect against stress-induced major depression, and hence, could serve as a resilience mechanism. In this review, we will summarize current knowledge about the functional relation of adult neurogenesis and stress in health and disease. A special focus will lie on the mechanisms underlying the cascades of events from prolonged high glucocorticoid concentrations to reduced numbers of newborn neurons. In addition to neurotransmitter and neurotrophic factor dysregulation, these mechanisms include immunomodulatory pathways, as well as microbiota changes influencing the gut-brain axis. Finally, we discuss recent findings delineating the role of adult neurogenesis in stress resilience.

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“…Li et al reported that the down-regulation of BIM was related to activation of TRKB in neuroblastoma cells (46). Regarding fluoxetineregulated BDNF with TRKB signalling (47,48), fluoxetine injection was associated with the down-regulation of BIM by TRKB signalling.…”

Section: Discussionmentioning

confidence: 99%

Differential Expression of BDNF and BIM in Streptozotocin-induced Diabetic Rat Retina After Fluoxetine Injection

Kim

Chung

Hwang

et al. 2021

In Vivo

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Background: Chronic diabetic retinopathy (DR) is a diabetic complication that causes blindness. Brainderived neurotrophic factor (BDNF) expression is induced by fluoxetine. We observed the effects of fluoxetine on a streptozotocin (STZ)-induced diabetic rat model in this study. Materials and Methods: Rats were divided into three groups: Control, diabetic (65 mg/kg STZ injection), and diabetic with fluoxetine injection (20 mg/kg/week, six times). Western blotting was performed using anti-BDNF and anti-hexaribonucleotide-binding protein-3. Expression of BCL2 apoptosis regulator-like protein 11 (BIM) was analysed using a reverse transcription-polymerase chain reaction. Results: BDNF levels were significantly higher in the diabetic group treated with fluoxetine than in the untreated diabetic group. BIM expression was higher in the diabetic group than in the control group. BIM gene expression was lower in fluoxetinetreated diabetic group than in the untreated diabetic group. Conclusion: Fluoxetine had an anti-apoptotic effect with upregulation of BDNF expression in retina of rats with STZinduced diabetes.Diabetic retinopathy (DR) is a complication of diabetes that causes blindness (1). Important mechanisms of blindness are macular edema and alteration of neovascularisation (2, 3). Vascular endothelial growth factor (VEGF) is the most effective mediator of DR progression (4). Anti-VEGF effects are associated with the regression of retinal neovascularisation (5) and anti-VEGF treatment is the most effective approach for DR therapy. However, some patients show poor response to this treatment (6). Thus, comprehension of the pathogenesis of DR is critical. Although DR is traditionally known as a vascular disease, some studies have shown that neuronal pathological changes occur in the retina, including physiological and structural alterations (7, 8).Brain-derived neurotrophic factor (BDNF) is a neuroprotective growth factor that affects neuronal cell proliferation and survival (9). BDNF binds to tropomyosin receptor kinase B (TRKB), which leads to nerve cell survival, repair, and development through the neurotrophic signalling pathway (10). BDNF has also been observed in retinal neuronal cells. BDNF is expressed in retinal ganglion cells (RGCs) and was found to play an important role in their survival in rats with streptozotocin (STZ)-induced diabetes (11). Cusato et al. reported that BDNF prevented cell death in the inner nuclear layer of the retina (12). Uzel et al. showed that BDNF is a good marker for the early diagnosis of DR (13).In a previous study, BDNF expression was induced by fluoxetine, a selective inhibitor of serotonin reuptake, to treat major depression (14). In this study, we analysed the expression of BDNF and BCL2 apoptosis regulator-like protein 11 (BIM) after fluoxetine injection in the STZinduced diabetes rat model to investigate the effect of fluoxetine on BDNF signalling. Materials and MethodsRat model of DR. All animal studies were approved by the Chosun University Institutional Animal Care and Use C...

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Antidepressant Drugs Correct the Imbalance Between proBDNF/p75NTR/Sortilin and Mature BDNF/TrkB in the Brain of Mice with Chronic Stress

Cited by 34 publications

References 39 publications

Neurotrophic Factor BDNF, Physiological Functions and Therapeutic Potential in Depression, Neurodegeneration and Brain Cancer

Neurotrophic Factor BDNF, Physiological Functions and Therapeutic Potential in Depression, Neurodegeneration and Brain Cancer

Stress-Related Dysfunction of Adult Hippocampal Neurogenesis—An Attempt for Understanding Resilience?

Differential Expression of BDNF and BIM in Streptozotocin-induced Diabetic Rat Retina After Fluoxetine Injection

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