Reemergence of ocular dominance plasticity during recovery from the effects of propranolol infused in kitten visual cortex.
Reemergence of ocular dominance plasticity during recovery from the effects of propranolol infused in kitten visual cortex.
复制标题
在小猫视觉皮层注射普萘洛尔的影响恢复过程中,眼部优势可塑性重新出现。
DOI:
10.1007/bf00249791
复制
发表时间:
1987
影响因子:
2
通讯作者:
Kasamatsu,T
中科院分区:
文献类型:
--
作者:
Shirokawa,T;Kasamatsu,T
We wanted to know whether ocular dominance plasticity can increase under the condition in which the number of available β 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 β 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 β adrenoreceptors 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 β adrenoreceptors for endogenous as well as exogenous NA.