Gene expression studies indicate that during activity-dependent development
al plasticity, N-methyl-D-aspartate receptor activation causes a Ca2+-depen
dent increase in expression of transcription factors and their downstream t
argets. The products of these plasticity genes then operate collectively to
bring about the structural and functional changes that underlie ocular dom
inance plasticity in visual cortex. Identifying and characterizing plastici
ty genes provides a tool for molecular dissection of the mechanisms involve
d. Members of second-messenger pathways identified in adult plasticity para
digms and elements of the transmission machinery are the first candidate pl
asticity genes tested for their role in activity-dependent developmental pl
asticity. Knockout mice with deletions of such genes have allowed analyzing
their function in the context of different systems and in different paradi
gms. Studies of mutant mice reveal that activity-dependent plasticity is no
t necessarily a unified phenomenon. The relative importance of a gene can v
ary with the context of its expression during different forms of plasticity
. Forward genetic screens provide additional new candidates for testing, so
me with well-defined cellular functions that provide insight into possible
plasticity mechanisms. (C) 1999 John Wiley & Sons, Inc.