The TNF-a signalling in the rapid plasticity of visual system following monocular enucleation.

Early CNS lesions are followed by rapid structural reorganization of circuits, usually related to functional brain recovery, whereas in adults, recovery is slow, with partial and anomalous plasticity. In parallel, focal lesions induce neuroinflammation that encourages the study of the dynamics between neuroplasticity mechanisms and immune activation in CNS injury context. TNF-α, a key proinflammatory cytokine that exerts its effects via TNF receptor subtype-1 (TNFR1) or -2 (TNFR2), can stimulate the glial release of trophic factors related to neuroplasticity.