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

Retrograde transport of NT-3 stimulated the reorganization of lumbar neural circuitry and synaptic connectivity remote to a thoracic SCI, along with improved behavioral recovery.

Induction of the fission of mitochondria-populating sensory axons is shown to be a novel biological action of neurotrophins.

Overexpression of the growth factor neurotrophin-3 helps to repair noise-induced damage in the mouse inner ear by promoting the regeneration of damaged synapses.

The K(+) uptake system KtrAB is controlled by an allosteric mechanism entirely new for membrane channels, which operates the channel gate over a 35 Å distance.

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.

Direct inhibition of pyridoxal phosphatase activity by 7,8-dihydroxyflavone indicates a pharmacological entry point into brain disorders associated with vitamin B6 deficiency.

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.

Surveying Mycobacterium tuberculosis tRNA modification leads to identification of a modification promoting Mtb pathogenesis.

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