We use culture on soft substrates to demonstrate a paxillin-linked bistable switch that governs the ability of newborn neurons to shift their lamellipodium morphology to one of two stable states, and to assume a neuritogenic state within a few hours. Our system recapitulates temporal and morphologic features observed in vivo. By contrast, when cells are grown on rigid substrates or when endocytosis is inhibited, neurons adopt the behavior of most migratory cells and paxillin becomes associated with cell-matrix or adhesion factors, exhibiting broad lamellipodia that delay neurite formation. Such biphasic neurite initiation emerges from an amplification loop enabling mutual inhibition of endocytosis by the adhesion machinery, and vice versa. Through this mechanism, newborn neurons can respond to the soft environments that dictate a phenotypic switch to allow neurite initiation.