Since learning in infancy has high efficiency, it could occur by a neural mechanism different from learning in adult. Imprinting behavior in birds is one of the suitable models to investigate the neural basis of juvenile learning. In imprinting behavior, the ability of learning is limited from the first to 4 days after hatching in chicks. This developmental stage is the critical period or sensitive period of imprinting behavior. During this critical period, the neural activity and NR2B expression are high in a telencephalic circuit which is responsible for the process of visual imprinting. When the expression of NR2B was suppressed in this neural circuit by RNA interference using shRNA, imprinting was inhibited. On the other hand, when NR2B-containing NMDA receptors (NR2B/NR1) expression was temporary enhanced at synaptic surface by treatment with a casein kinase 2 inhibitor, chicks could be imprinted by a shorter training. In imprinted chick, synaptic current and cell surface expression of AMPA receptors and NR2B/NR1 were upregulated in the cells constituting the telencephalic circuit of imprinting. Enhancement of surface NR2B/NR1 expression could be induced even by the shorter training which is too weak to imprint chicks. Moreover, activation of NR2B/NR1 mediated its own expression on the neural surface, through degradation of synaptic p35 molecules. These results indicate that NR2B dependent neural plastic changes lead to an efficient learning characteristic of juvenile period. Now we are pursuing the neural mechanism which enables developmental changes of NR2B expression.