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.

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

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

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

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

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.

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

Structural and functional striatal synaptic plasticity abnormalities occur early in a sensitive developmental period, representing a potential unique endophenotypic traits that increase the risk of manifesting clinical symptoms in DYT1 mutation carriers.