scholarly journals Prenatal stress alters hippocampal synaptic plasticity in young rat offspring through preventing the proteolytic conversion of pro-brain-derived neurotrophic factor (BDNF) to mature BDNF

2012 ◽  
Vol 590 (4) ◽  
pp. 991-1010 ◽  
Author(s):  
Che-Ming Yeh ◽  
Chiung-Chun Huang ◽  
Kuei-Sen Hsu
Keyword(s):  
Synaptic Plasticity ◽  
Prenatal Stress ◽  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor ◽  
Rat Offspring ◽  
Hippocampal Synaptic Plasticity ◽  
Young Rat

Prenatal stress modifies hippocampal synaptic plasticity and spatial learning in young rat offspring

Hippocampus ◽  
2006 ◽  
Vol 16 (5) ◽  
pp. 431-436 ◽  
Author(s):  
Jianli Yang ◽  
Huili Han ◽  
Jun Cao ◽  
Lingjiang Li ◽  
Lin Xu
Keyword(s):  
Synaptic Plasticity ◽  
Spatial Learning ◽  
Prenatal Stress ◽  
Rat Offspring ◽  
Hippocampal Synaptic Plasticity ◽  
Young Rat

scholarly journals Brain-Derived Neurotrophic Factor-Induced Gene Expression Reveals Novel Actions of VGF in Hippocampal Synaptic Plasticity

2003 ◽  
Vol 23 (34) ◽  
pp. 10800-10808 ◽  
Author(s):  
Janet Alder ◽  
Smita Thakker-Varia ◽  
Debra A. Bangasser ◽  
May Kuroiwa ◽  
Mark R. Plummer ◽  
...  
Keyword(s):  
Gene Expression ◽  
Synaptic Plasticity ◽  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor ◽  
Hippocampal Synaptic Plasticity

Cellular and molecular mechanisms of the brain-derived neurotrophic factor in physiological and pathological conditions

2016 ◽  
Vol 131 (2) ◽  
pp. 123-138 ◽  
Author(s):  
Veronica Begni ◽  
Marco Andrea Riva ◽  
Annamaria Cattaneo
Keyword(s):  
Synaptic Plasticity ◽  
Stress Response ◽  
Neurotrophic Factor ◽  
Molecular Mechanisms ◽  
Depressive Disorders ◽  
Brain Derived Neurotrophic Factor ◽  
Mitogen Activated Protein Kinase ◽  
Bdnf Expression ◽  
Pathological Conditions ◽  
Wide Range

Brain-derived neurotrophic factor (BDNF) is a neurotrophin that plays a key role in the central nervous system, promoting synaptic plasticity, neurogenesis and neuroprotection. The BDNF gene structure is very complex and consists of multiple 5′-non-coding exons, which give rise to differently spliced transcripts, and one coding exon at the 3′-end. These multiple transcripts, together with the complex transcriptional regulatory machinery, lead to a complex and fine regulation of BDNF expression that can be tissue and stimulus specific. BDNF effects are mainly mediated by the high-affinity, tropomyosin-related, kinase B receptor and involve the activation of several downstream cascades, including the mitogen-activated protein kinase, phospholipase C-γ and phosphoinositide-3-kinase pathways. BDNF exerts a wide range of effects on neuronal function, including the modulation of activity-dependent synaptic plasticity and neurogenesis. Importantly, alterations in BDNF expression and function are involved in different brain disorders and represent a major downstream mechanism for stress response, which has important implications in psychiatric diseases, such as major depressive disorders and schizophrenia. In the present review, we have summarized the main features of BDNF in relation to neuronal plasticity, stress response and pathological conditions, and discussed the role of BDNF as a possible target for pharmacological and non-pharmacological treatments in the context of psychiatric illnesses.

The role of brain-derived neurotrophic factor and the neurotrophin receptor p75NTR in age-related brain atrophy and the transition to Alzheimer’s disease

2022 ◽  
Vol 0 (0) ◽  
Author(s):  
Shaun Cade ◽  
Xin-Fu Zhou ◽  
Larisa Bobrovskaya
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Synaptic Plasticity ◽  
Neurotrophic Factor ◽  
Molecular Mechanisms ◽  
Brain Derived Neurotrophic Factor ◽  
Neurotrophin Receptor ◽  
Current Evidence ◽  
Synaptic Dysfunction ◽  
Age Related

Abstract Alzheimer’s disease is a neurodegenerative condition that is potentially mediated by synaptic dysfunction before the onset of cognitive impairments. The disease mostly affects elderly people and there is currently no therapeutic which halts its progression. One therapeutic strategy for Alzheimer’s disease is to regenerate lost synapses by targeting mechanisms involved in synaptic plasticity. This strategy has led to promising drug candidates in clinical trials, but further progress needs to be made. An unresolved problem of Alzheimer’s disease is to identify the molecular mechanisms that render the aged brain susceptible to synaptic dysfunction. Understanding this susceptibility may identify drug targets which could halt, or even reverse, the disease’s progression. Brain derived neurotrophic factor is a neurotrophin expressed in the brain previously implicated in Alzheimer’s disease due to its involvement in synaptic plasticity. Low levels of the protein increase susceptibility to the disease and post-mortem studies consistently show reductions in its expression. A desirable therapeutic approach for Alzheimer’s disease is to stimulate the expression of brain derived neurotrophic factor and potentially regenerate lost synapses. However, synthesis and secretion of the protein are regulated by complex activity-dependent mechanisms within neurons, which makes this approach challenging. Moreover, the protein is synthesised as a precursor which exerts the opposite effect of its mature form through the neurotrophin receptor p75NTR. This review will evaluate current evidence on how age-related alterations in the synthesis, processing and signalling of brain derived neurotrophic factor may increase the risk of Alzheimer’s disease.

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