Reemergence of ocular dominance plasticity during recovery from the effects of propranolol infused in kitten visual cortex.

We wanted to know whether ocular dominance plasticity can increase under the condition in which the number of available beta adrenoreceptors is expected to increase within kitten visual cortex. We adopted a paradigm in which monocular lid suture was carried out some time after the termination of direct infusion of the cortex with a beta adrenoreceptor antagonist. A significant change in ocular dominance was obtained as shown by a decrease in binocular cortical neurons, when time interval between the end of the d,l-propranolol infusion and the start of monocular deprivation was one week. With a 3-week interval (the longest tested), an even greater change in ocular dominance was evident. This consisted of a marked decrease in binocular neurons and a shift in ocular dominance toward the nondeprived eye. In a control study an inert stereoisomer, d-propranolol, did not block the ocular dominance shift. These results were interpreted as suggesting that the level of ocular dominance plasticity becomes high in parallel to an expected increase in availability of beta adrenoceptors for endogenous noradrenaline (NA). We next asked whether it is possible to accelerate or decelerate the naturally occurring recovery of ocular dominance plasticity. When either NA or tunicamycin (an inhibitor of protein glycosylation) was infused into the same cortical area immediately after the end of the propranolol infusion, opposite effects were observed: exogenous NA accelerated the recovery of the shift in ocular dominance and tunicamycin suppressed it. When tunicamycin infusion was delayed by one week, however, its suppressive effect was negligible. Thus, the restoration of ocular dominance plasticity seems to occur in parallel to an increase in the availability of beta adrenoreceptors for endogenous as well as exogenous NA.