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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.
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CA3-specific deletion of BDNF results in deficits in circuits that process social cues from familiar conspecifics.
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findings suggest that reductions in concentrations of BDNF results in altered status of excitability and excitation/inhibition imbalance.
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It has been shown that the Wnt3a/beta-catenin/BDNF axis in the spinal neural circuit plays an important role in regulating capsaicin-induced pain.
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High BDNF expression is associated with anxiety and memory disorders in Huntington's disease.
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These data suggested an anxiogenic- and antidepressant-like phenotype of ELA2 knockout, possibly associated with increased levels of BDNF in the prefrontal cortex.
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Prep1 deficiency alters olfactory morpho-functional integrity and olfaction-mediated eating behavior by affecting BDNF-TrkB signaling.
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Electroconvulsive therapy in an animal model of depression increases BDNF expression in the cerebral cortex.
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results provide evidence that adaptations in cortical (mPFC) BDNF activity resulting from chronic ethanol exposure play a role in mediating excessive ethanol drinking associated with dependence.
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These results provide further evidence that Bdnf splice variants generate a spatial code that mediates the local actions of BDNF in distinct dendritic compartments on structural and functional plasticity.
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Study demonstrated up-regulation of miR-210-3p by MPP+ reduces the brain-derived neurotrophic factor production and contributes to the dopaminergic neuron damage.
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we found that the effect of genipin on PRS mice occurs through DNA demethylation by inhibiting DNA methyltransferase 1 (DNMT1), normalizing the expression of reduced brain-derived neurotrophic factor (BDNF) in the hippocampus
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glucose administration increased phosphorylated Akt, phosphorylated CREB, exon 1- and exon 4-specific BDNF transcripts, and FGF1 transcripts that are associated with the epigenetic changes.
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the BDNF-EPO-Shh novel-signaling pathway underlies the regulation of inflammatory responses.
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BDNF regulates the timing of neurodevelopment via a novel mechanism of extranuclear sequestration of NFATc4 in Golgi. This leads to accelerated derepression of an NFI temporal occupancy gene program in cerebellar granule cells that includes Bdnf itself, revealing an autoregulatory loop within the program driven by BDNF and NFATc4.
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An acute bout of exercise can recover BDNF-TrkB signalling in the prefrontal cortex of obese, glucose intolerant mice.
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Results give strong evidence for a cell type-specific brain derived neurotrophin factor (BDNF), TrkB signaling in modulating neuronal architecture. Study propose that a BDNF-independent transactivation of TrkB receptor may be able to compensate the lack of BDNF signaling to modulate neuronal morphology in a cell type-specific manner.
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These results suggest that psychological stress during gestation can induce long-term mood alterations in pregnant mice, which may correlate with changes in miR-206-3p and BDNF expression in the hippocampus, mPFC and amygdala.
