Figure 9. SFK is a primary target in ethanol disruption of CGN axon outgrowth.

Axon outgrowth begins when diverse ligands bind to their unique receptors; a membrane-bound receptor for NAP has not yet been identified. The ligand-bound receptors activate SFK, thereby activating its downstream signaling molecules, Cas and ERK1/2. Activation of the Cas and ERK1/2 kinases is coupled to remodeling of the cytoskeleton and axon outgrowth. Ethanol inhibits ligand stimulation of axon outgrowth by blocking ligand activation of SFK. BDNF stimulates axon outgrowth and activates ERK1/2 without activating SFK, and ethanol does not inhibit BDNF-mediated axon outgrowth or activation of ERK1/2. Thus, SFK appears to be a primary target in ethanol inhibition of axon outgrowth stimulated by diverse axon guidance molecules and growth factors.