ABSTRACT
Although lateralization is a core feature of information processing of vertebrate brains, there is no model which can explain how ontogenetic mechanisms lead to an adult asymmetric functional architecture. While the very early appearance o f embryonic asymmetries and the heritability of specific lateralization patterns suggest a genetic founda tion, a high degree o f plasticity highlights the critical role of environmental factors. The avian visual system demonstrates that the formation o f neuronal asymmetries can be caused by sensory stimulation that is asymmetrically experienced. Monocular deprivation or intraocu lar applications o f tetrodotoxin or BD N F suggest that lateralization develops via activity-dependent differentiation of brain circuits. A brief period of visual asymmetry in prehatch birds, resulting from a genetically determined head turning bias, triggers asymmet ric differentiation processes in both hemispheres which gain significance during posthatch maturation. During this time, functional dominance of the right eye/left hemisphere for visual feature analysis develops, and morphological asymmetries in the tectofugal pathway differentiate into an adult phenotype.
