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Authors identify a potential role for BDNF in PWS that requires further exploration and may have therapeutic relevance for this complex neuro-behavioral disorder.
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FTO affects hippocampal function by regulation of BDNF processing.
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The data suggest that CADPS2-mediated secretion of BDNF/NT-3 may be involved in development and maturation of synapses and in the balance between inhibitory and excitatory synapses.
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Bdnf removal from the tongue or from all structures in adult mice impacts the way taste nerves project to the first central relay. Deletion of Bdnf from the tongue and from all tissues led to a progressively greater expansion of terminal fields. This demonstrates, for the first time, that BDNF is necessary for the normal maintenance of central gustatory circuits at adulthood.
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Data suggest that response similar to nicotine withdrawal or/and hypoxia induced by childhood chronic asthma enhances the BDNF-Cdc42/RhoA signaling pathway and activates cofilin1, leading to the remodeling of actin, causing the loss of dendritic spines and atrophy of dendrites, eventually resulting in behavioral alterations.
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Our findings show that disruption of BDNF from specific promoters leads to distinct body composition effects, with disruption from promoters I or II, but not IV or VI, inducing obesity.
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Endogenous BDNF might be protective against apoptosis through GADD153 suppression and steatosis via SREBP-1c suppression during ER stress
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The BDNF Met prodomain renders ventral CA1 - prelimbic projection neurons underdeveloped, preventing their capacity for subsequent circuit modulation necessary for fear extinction.
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BDNF gene in mice fed high-fat diet was under-expressed by 0.30 fold with respect to chow-fed mice after 3 months of dietary intervention.
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Results provide evidence of a causal relationship between reduced BDNF function in hippocampus and the anxiety susceptibility of aged mice.
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Chronic unpredictable mild stress (CUMS) induced depressive-like behaviors and stimulated changes in brain regions expressing different BDNF levels. Depressive-like behaviors and region-specific BOLD activity in BDNF(tm1Krj/J) mice were consistent with those in wild-type CUMS-exposed mice. Findings suggested a potential central role of BDNF expression in functional changes in the brain.
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Central BDNF, especially subfornical organ BDNF is involved in the maintenance of basal blood pressure and in augmentation of hypertensive response to angiotensin II.
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The data of this study demonstrated that 24 h after fear conditioning, BDNF+/- mice exhibited an impaired fear memory expression.
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This study demonstrated that Brain-derived neurotrophic factor derived from sensory neurons plays a critical role in chronic pain.
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Deficiency in MyD88 was associated with decreased BDNF expression. Furthermore, the authors identified a valid kappaB-binding site in the BDNF promoter, consistent with activation of NF-kappaB induced by inflammation.
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The activation of PKCalpha during plasticity requires both NMDA receptor Ca(2+) flux and autocrine brain-derived neurotrophic factor (BDNF)-TrkB signaling, two pathways that differ vastly in their spatiotemporal scales of signaling
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BDNF val66met polymorphism modulates the effects of developmental EtOH exposure on hippocampus and anxiety-like behavior.
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Results show that BDNF haploinsufficiency substantially decreases the neuroprotective effect of the steroid mifepristone on Purkinje neurons. This suggests that a full expression of BDNF is critical to prevent the neurotoxicity induced by the GABAergic network activity.
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Closer examination of genes implicated in the mechanisms of neuroplasticity, such as the NMDA and AMPA subunits and the BDNF pathway, reveal how wild-type mice upregulate many of these genes in response to stress, but Met allele carriers fail to do so.
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This study found that BDNF deletion in the adult altered few itch or acute and chronic pain behaviors, beyond sexually dimorphic phenotypes in the tail immersion, histamine, and formalin tests.