A phenomenon often seen in early normal development, and as with axonal proliferation occurring before birth, where axons extend farther, or to more places or terminal zones, than they will at maturity. They then refine their connections by retracting. Examples include the retraction of corpus callosum collaterals and the elimination of cortical-cortical connections (e.g., layer 5 in the visual cortex eliminates projections to the spinal cord). Despite its ubiquity as a widespread regressive phenomenon in the developing brain that helps sculpt the pattern of neuronal connections, the underlying mechanisms are incompletely understood, as with synapse elimination. Consequently, much research on axon retraction has focused on the neuromuscular junction because of its relative accessibility and simplicity, where it is thought that axons compete for some neurotrophic growth factors, with the ‘losers’ retracting (the so-called neurotrophic hypothesis). The best-studied neurotrophic factor is the nerve growth factor (NGF), which is essential for the survival and differentiation of most sympathetic neurons and many, but not all, sensory neurons. It has no known effect on motoneurons. Thus, motoneurons must depend on another kind of neurotrophic factor, and in this respect the glial-derived neurotrophic factor (GDNF) has been proposed. Other factors include brain-derived neurotrophic factor, fibroblast growth factors, neurotrophin-3, neurotrophin-4/5, glial cell derived neurotrophic factor, leukocyte inducing factor (also called leukaemia inhibiting factor), ciliary neurotrophic factor, and insulin-like growth factors.
See Axon, Brain derived neurotrophic factor (BDNF), Cerebral cortex (development), Corpus callosum, Fibroblast growth factor (FGF), Glial-derived neurotrophic factor (GDNF), Motoneuron, Nerve growth factor (NGF), Neuromuscular junction, Neurotrophic growth factor (NGF), Neurotrophin-NT3, Plasticity (neural), Polyinnervation to monoinnervation, Quantitative and qualitative regressions, Regressive event, Synapse elimination, Visual cortex