Difference and relationship between plastic synapse of sensitive period and that of after effect in the visual cortex.

自1963年威塞尔和Hubel的开创性工作以来，在敏感期观察到的眼球剂量可塑性的调节涉及(I)活动依赖机制和(Ii)神经化学基础。我们认为，中枢去甲肾上腺素系统作为主要的神经化学基础，在眼优势可塑性的调节中起着至关重要的作用。最近的电子显微镜研究表明，猫视皮层的星形胶质细胞表达β-肾上腺素能受体。因此，我们认为去甲肾上腺素(NA)的作用可能部分由星形胶质细胞功能介导，未成熟的星形胶质细胞可能整合了活动依赖机制和神经化学基础。我们已经证明，一种胶质毒素抑制了眼优势可塑性。这种神经胶质受累可能是敏感期可塑性所特有的，而不是后遗症。我们使用自波栅化以来的适当漂移来研究后效。在被检查的第17区，50%的细胞显示后效。较低的后遗症频率似乎取决于麻醉和瘫痪。已有研究表明，在麻醉和麻痹条件下，眼优势可塑性是冻结的。尽管这些发现可能是相互关联的，但我们没有检测到NA诱导引起的细胞频率的增加。对单眼剥夺的小猫的实验表明，剥夺眼的条件反射不会引起正常眼的后遗症，这表明在敏感期，后遗症的突触受到视觉环境的影响。

Since the pioneering work by Wiesel and Hubel in 1963, involvements of (i) the activity-dependent mechanism and (ii) the neurochemical basis, have been suggested in the regulation of the ocular doinance plasticity observed during the sensitive period. We have proposed that the central noradrenergic system plays a crucial role in the regulation of the ocular dominance plasticity as a major neurochemical basis. Recent electron microscopic studies showed that astrocytes in kitten visual cortex express beta-adrenergic receptors. Thus, we consider a possibility that the action of noradrenaline (NA) is partially mediated by the astrocytic function and immature astrocytes may integrate the activity-dependent mechanism and the neurochemical basis. We have shown that a gliotoxin suppressed the ocular dominance plasticity. This glial involvement may be unique for the sensitive period plasticity not for the aftereffect. We studied after effects using adequate drifting since wave grating.Fifty percent of cells in area 17 examined showed aftereffect. The lower frequency of aftereffect seems to depend on the anesthesia and paralysis. It has priviously been demonstrated that ocular dominance plasticity is freezed under anesthetized and paralyzed conditions. Although, these finding may be correlated each other, we could not detect the increase of frequency of cells showing aftereffect by the NA indusion. Experiments with the monocularly deprived kitten showed that the conditioning of the deprived eye never induced aftereffect of the normal eye, suggested that synapses of aftereffect are affected by visual environment during the sensitive period.