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.
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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
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发表时间:
1987
影响因子:
2
通讯作者:
Kasamatsu,T
Kasamatsu,T
中科院分区:
医学4区
文献类型:
--
作者:
Shirokawa,T;Kasamatsu,T

文献摘要

相似文献

我们想知道在小猫视觉皮层内可用 β 肾上腺素受体数量预计增加的情况下,眼部优势可塑性是否会增加。我们采用了一种范例,其中在皮质直接输注β肾上腺素受体拮抗剂终止一段时间后进行单眼睑缝合。当 d,l-普萘洛尔输注结束和单眼剥夺开始之间的时间间隔为一周时,双眼皮质神经元减少表明,眼优势发生显着变化。间隔 3 周(最长的测试时间)后,优势眼发生了更大的变化。这包括双眼神经元的显着减少以及眼部优势向非剥夺眼的转变。在一项对照研究中,惰性立体异构体 d-普萘洛尔并不能阻止眼部优势转移。这些结果被解释为表明眼优势可塑性水平变高,同时内源性去甲肾上腺素(NA)的β肾上腺素受体的可用性预期增加。接下来我们询问是否有可能加速或减缓眼睛优势可塑性的自然恢复。当普萘洛尔输注结束后立即将 NA 或衣霉素(蛋白质糖基化抑制剂)注射到同一皮质区域时,观察到相反的效果:外源性 NA 加速了眼优势转变的恢复,而衣霉素则抑制了它。然而,当衣霉素输注延迟一周时,其抑制作用可以忽略不计。因此,眼优势可塑性的恢复似乎与内源性和外源性 NA 的 β 肾上腺素受体可用性的增加同时发生。
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.