A5032686473- Nerve injury and regeneration
- Neurogenesis and neuroplasticity mechanisms
- Neuroscience and Neuropharmacology Research
- Signaling Pathways in Disease
- Neuroinflammation and Neurodegeneration Mechanisms
- Memory and Neural Mechanisms
- Autism Spectrum Disorder Research
- Cellular transport and secretion
- Genetics and Neurodevelopmental Disorders
- Receptor Mechanisms and Signaling
- Neuropeptides and Animal Physiology
- Axon Guidance and Neuronal Signaling
- Mitochondrial Function and Pathology
- Alzheimer's disease research and treatments
- Viral Infectious Diseases and Gene Expression in Insects
- RNA Interference and Gene Delivery
- Nuclear Receptors and Signaling
- ATP Synthase and ATPases Research
- Retinal Development and Disorders
- Calpain Protease Function and Regulation
- Pain Mechanisms and Treatments
- Cholinesterase and Neurodegenerative Diseases
- Ubiquitin and proteasome pathways
- Cancer-related molecular mechanisms research
- 14-3-3 protein interactions
Shandong University
2013-2024
Qilu Hospital of Shandong University
2009-2024
First Affiliated Hospital of Zhengzhou University
2024
Shuguang Hospital
2021-2023
Shanghai University of Traditional Chinese Medicine
2021-2023
Shandong University of Traditional Chinese Medicine
2021-2023
Center for Excellence in Education
2015
Cornell University
2004-2009
King University
2009
Rockefeller University
2006
A common single-nucleotide polymorphism in the brain-derived neurotrophic factor (BDNF) gene, a methionine (Met) substitution for valine (Val) at codon 66 (Val66Met), is associated with alterations brain anatomy and memory, but its relevance to clinical disorders unclear. We generated variant BDNF mouse (BDNF Met/Met ) that reproduces phenotypic hallmarks humans allele. Met was expressed normal levels, secretion from neurons defective. When placed stressful settings, mice exhibited increased...
Brain-derived neurotrophic factor (BDNF) is best characterized for critical roles in neuronal survival, differentiation, and synaptic modulation mediated by the TrkB receptor tyrosine kinase. Developmentally regulated death signaling BDNF has also been demonstrated via activation of p75 NTR . Because recent studies suggest that proNGF, precursor form NGF, more active than mature NGF inducing apoptosis after binding to a coreceptor, sortilin, we asked whether (proBDNF) proapoptotic ligand...
Brain-derived neurotrophic factor (BDNF), after activity-dependent secretion from neurons, modulates critical nervous system functions. Recently, a variant in the human bdnf gene, resulting valine to methionine substitution prodomain, has been shown lead defective regulated neurons and memory impairment. Here, we report novel function for Vps10p domain protein, sortilin, controlling BDNF sorting secretory pathway. Sortilin interacts specifically with region encompassing colocalizes granules...
Brain-derived neurotrophic factor (BDNF) plays important roles in cell survival, neural plasticity, learning, and stress regulation. However, whether the recently found human BDNF Val66Met ( Met ) polymorphism could alter vulnerability remains controversial. More importantly, molecular structural mechanisms underlying interaction between are unclear. We that heterozygous +/Met mice displayed hypothalamic-pituitary-adrenal axis hyperreactivity, increased depressive-like anxiety-like...
Neurotrophins, such as NGF and BDNF, activate Trk receptor tyrosine kinases through dimerization at the cell surface followed by autophosphorylation intracellular signaling. It has been shown that activation of can also occur via a G-protein-coupled (GPCR) mechanism, without involvement neurotrophins. Two GPCR ligands, adenosine pituitary adenylate cyclase-activating polypeptide (PACAP), activity to increase survival neural cells stimulation Akt activity. To investigate mechanism...
Neurogenesis, the division, migration, and differentiation of new neurons, occurs throughout life. Brain derived neurotrophic factor (BDNF) has been identified as a potential signaling molecule regulating neurogenesis in subventricular zone (SVZ), but its functional consequences vivo have not well defined. We report marked unexpected deficits survival proliferation newly born cells adult knock-in mice containing variant form BDNF [a valine (Val) to methionine (Met) substitution at position...
Brain-derived neurotrophic factor (BDNF) plays important roles in activity-dependent plasticity processes, such as long-term potentiation, learning, and memory. The recently reported human BDNF Val66Met (BDNF Met ) polymorphism has been shown to lead altered hippocampal volume impaired hippocampal-dependent memory is associated with a variety of neuropsychiatric disorders. There are few studies, however, that investigate the effect on hippocampal-independent processes. A conditioned taste...
Abstract Several genome- and proteome-wide studies have associated transcription translation changes of CRMP2 (collapsing response mediator protein 2) with psychiatric disorders, yet little is known about its function in the developing or adult mammalian brain vivo . Here we show that brain-specific Crmp2 knockout (cKO) mice display molecular, cellular, structural behavioural deficits, many which are reminiscent neural features symptoms schizophrenia. cKO exhibit enlarged ventricles impaired...
Appropriate mitochondrial transport and distribution are essential for neurons because of the high energy Ca(2+) buffering requirements at synapses. Brain-derived neurotrophic factor (BDNF) plays an role in regulating synaptic transmission plasticity. However, whether how BDNF can regulate still unclear. Here, we find that cultured hippocampal neurons, application 15 min decreased percentage moving mitochondria axons, a process dependent on activation TrkB receptor its downstream PI3K...
Endocytic trafficking of signaling receptors to alternate intracellular pathways has been shown lead diverse biological consequences. In this study, we report that two neurotrophin (tropomyosin-related kinase TrkA and TrkB) traverse divergent endocytic after binding their respective ligands (nerve growth factor brain-derived neurotrophic factor). We provide evidence in neurosecretory cells neurons predominantly recycle back the cell surface a ligand-dependent manner. have identified specific...
Brain-derived neurotrophic factor (BDNF) plays an important role in the activity-dependent regulation of synaptic structure and function via tropomyosin related kinase B (TrkB) receptor activation. However, whether BDNF could regulate TrkB levels at synapse during long-term potentiation (LTP) is still unknown. We show cultured rat hippocampal neurons that chemical LTP (cLTP) stimuli selectively promote endocytic recycling BDNF-dependent full-length (TrkB-FL) receptors, but not isoform T1...
Brain-derived neurotrophic factor (BDNF) and its receptor, tropomyosin-related kinase receptor B (TrkB), play a critical role in activity-dependent plasticity processes such as long-term potentiation, learning, memory. It has been shown that BDNF exerts different or even opposite effects on behavior depending the neural circuit. However, detailed of memory process basis location not fully understood. Here, we aim to investigate regional specific involvement BDNF/TrkB hippocampal-independent...
Brain-derived neurotrophic factor (BDNF) is a key regulator of hippocampal synaptic plasticity in the developing and adult nervous system. It can be released from pyramidal neuron dendrites an activity-dependent manner has therefore been suggested to serve as signal that provides retrograde intercellular communication necessary for Hebbian hippocampal-dependent learning. Although much learned about BDNF function by field stimulation neurons, it not known whether moderate action...
Actin dynamics provide an important mechanism for the modification of synaptic plasticity, which is regulated by actin depolymerizing factor (ADF)/cofilin. However, role cofilin in memory extinction process still unclear. Here, we observed that conditioned taste aversive (CTA) led to temporally enhanced ADF/cofilin activity infralimbic cortex (IrL) rats. Moreover, elevating IrL could accelerate CTA facilitating AMPAR surface recruitment, whereas inhibition abolished trafficking and impaired...