Brain-derived neurotrophic factor (BDNF)/TrkB.T1 signaling contributes to astrocyte morphological maturation, with implications for neuronal synaptogenesis and function and astrocyte functional maturation.

The antimanic action of lithium requires BDNF-TrkB signaling coupled with enhanced dynamin-dependent endocytosis of AMPARs as a potential mechanism underlying the therapeutic effects.

In mouse models of Rett syndrome, the impaired cell autonomous BDNF feed forward signaling pathway results in abnormalities in neurite outgrowth and synapse formation in excitatory neurons.

RbFox1 upregulation modulates the expression of hundreds of genes but only dysregulation of the TrkB.T1 receptor isoform expression causes BDNF-dependent LTP impairments.

A potential link between metabolic changes resulting from exercise and gene expression in the brain has been revealed.

An evolutionarily conserved neuron-specific and stimulus-dependent enhancer region downstream of the Bdnf exon III regulates the expression of Bdnf transcripts starting from the upstream 5' exons.

Oligodendrocytes are actively engaged in the precise control of synaptic functions in the CNS through activity-dependent BDNF signaling.

Brain-derived neurotrophic factor signaling plays a causal role in female-typical social behavior and modulates oxytocin neuron gene expression.

Loss of MeCP2 function negatively impacts Tet1 and CTCF binding thereby negatively impacting learning-dependent DNA methylation and alternative splicing regulation.

The innervation of the mammary gland is controlled by opposing effects of neurotrophic and repulsive factors and, once trophic signaling is inhibited the repulsive factors, may promote axonal pruning.