Kasamatsu T, Watabe K, Heggelund P, Schöller E
Neurosci Res. 1985 Jun;2(5):365-86. doi: 10.1016/0168-0102(85)90047-1.
It has been proposed that the presence of noradrenaline (NA)-containing terminals and NA-related receptors within the visual cortex is necessary to maintain the high level of neuronal plasticity in the immature visual cortex of kittens. In the present study we wanted to show whether electrical stimulation of the locus coeruleus (LC), which contains the somata of these cortical NA fibers, can restore neuronal plasticity to the normally aplastic visual cortex of juvenile and adult cats. We consistently found a significant loss of binocular cells in the visual cortex of mature animals which had monocular vision for only 12 h dispersed over 6 days (2 h a day, otherwise kept in the dark) in combination with concurrent LC stimulation. This result was interpreted as indicating that endogenous NA released from NA terminals restored susceptibility to monocular vision in the mature visual cortex. We next examined how long the restored plasticity lasts in the same animals after the LC stimulation was ended. The animals revived from the first recording session were either returned to the same daily schedule of brief monocular exposure (light/dark = 2/22 h) as before, or subjected to the usual monocular lid suture and kept in a cat colony environment (light/dark = 16/8 h). The LC electrodes had been removed and no more electrical stimulation was delivered at this stage. In the animals subjected to reiteration of brief monocular exposure, the state of reduced binocularity gradually returned to normal over a period of 2-3 weeks after stopping LC stimulation. We calculated that the revived plasticity disappeared at an average rate of a 22% loss every 7 days. This result sharply contrasted with the result obtained in the animals subjected to usual monocular lid suture. In this test the state of reduced binocularity continued for at least the next 3 weeks, suggesting that the restored plasticity was sustained throughout a period of 3 weeks (longest term tested). The different results obtained in the two paradigms may be explained by the different strength of binocular imbalance in the two tests imposed on the visual cortex in which neuronal plasticity was restored partially.
有人提出，在视觉皮层中存在含去甲肾上腺素（NA）的终末和与NA相关的受体，对于维持小猫未成熟视觉皮层中高水平的神经元可塑性是必要的。在本研究中，我们想表明，电刺激蓝斑（LC）——其中包含这些皮层NA纤维的胞体——是否能恢复幼年和成年猫正常无可塑性的视觉皮层的神经元可塑性。我们持续发现，在成熟动物的视觉皮层中，双眼细胞显著减少，这些动物在6天内仅单眼视觉12小时（每天2小时，其他时间置于黑暗中），同时进行LC刺激。这一结果被解释为表明从NA终末释放的内源性NA恢复了成熟视觉皮层对单眼视觉的敏感性。接下来，我们研究了在LC刺激结束后，恢复的可塑性在同一动物中能持续多长时间。从第一次记录 session 苏醒的动物，要么恢复到之前相同的每日短暂单眼暴露时间表（光照/黑暗 = 2/22小时），要么进行通常的单眼眼睑缝合，并饲养在猫群环境中（光照/黑暗 = 16/8小时）。此时LC电极已移除，不再进行电刺激。在经历短暂单眼暴露重复的动物中，双眼性降低的状态在停止LC刺激后的2 - 3周内逐渐恢复正常。我们计算出，恢复的可塑性以每7天平均损失22%的速度消失。这一结果与进行通常单眼眼睑缝合的动物所得到的结果形成鲜明对比。在这个测试中，双眼性降低的状态至少持续了接下来的3周，表明恢复的可塑性在3周（测试的最长时间）内持续存在。在这两种范式中获得的不同结果，可能是由于在部分恢复神经元可塑性的视觉皮层上施加的两种测试中，双眼不平衡的强度不同所致。
