Based on a theory that a norepinephrine-stimulated cascade of events resulting in an increase of intracellular cyclic adenosine 3',5'-monophosphate (cAMP) modulates the state of plasticity for the receptive field property of visual cortical neurons, we have followed the ontogenetic changes in cAMP-stimulated phosphorylation of proteins in whole homogenates obtained from developing visual cortices of cats. In vitro phosphorylation was assayed with and without cAMP and the cAMP-dependent protein kinase, and the phosphoproteins separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis were counted for 32P incorporated from [gamma-32P]ATP. It was found that the regulatory subunits of the cAMP-dependent protein kinase are present and fully active by birth, whereas the synapsin content increases at a rate concomitant with synaptogenesis. These ontogenetic developments are not influenced by dark rearing (DR) from birth, a procedure which postpones the onset of the critical period (CP) for plasticity. By contrast, the cAMP-stimulatable phosphorylation of microtubule-associated protein 2 (MAP 2), which under normal rearing conditions increases from birth to the second month, is strongly modulated by the presence of light in the environment. After DR for various periods, kittens were subsequently exposed to light so as to trigger the onset of the CP that had been postponed. A few hours of light were sufficient to cause a large increase in the in vitro phosphorylation of MAP 2. This effect is not observed in the auditory cortex or the lateral geniculate nucleus of the same animals, or in the visual cortex of normally reared cats which were then dark reared in adulthood. But this effect was seen in the visual cortices of cats following 5 months of DR from birth, animals which by chronological age have passed the CP, presumably because the onset of the CP was extended by the DR procedure. The cAMP-dependent phosphorylation of MAP 2 (and its dephosphorylation) may be an important factor for determining the state of plasticity in the CP through its affecting the dendritic cytoskeletal organization involving tubulin and actin.