Lewis T L, Maurer D, Brent H P
Can J Psychol. 1989 Jun;43(2):121-40. doi: 10.1037/h0084225.
Ten years ago we proposed that the limitations on young infants' vision might be caused by an immature Y-pathway through the cortex, while their abilities might be mediated by an X-pathway to the cortex and by Y- and/or W-pathways to the superior colliculus and pretectum (Maurer & Lewis, 1979). Although that explanation was too simple overall, it fits well with what is known about asymmetrical optokinetic nystagmus, viz. the difficulty in eliciting OKN to patterns moving from the nasal field toward the temporal field. In this paper, we describe the development of symmetrical OKN, its alteration by early deprivation from cataract, and its physiological basis. We then suggest that, for primates, an explanation based on projections through the magnocellular versus parvocellular layers of the lateral geniculate nucleus may be more appropriate than one based on X-, Y-, and W-cells.
十年前，我们提出，幼儿视力受限可能是由于通过皮层的Y通路不成熟所致，而他们的能力可能是由通向皮层的X通路以及通向中脑上丘和顶盖前区的Y和/或W通路介导的（莫勒和刘易斯，1979）。尽管总体而言，这种解释过于简单，但它与已知的不对称视动性眼震情况非常吻合，即难以诱发对从鼻侧视野向颞侧视野移动的图案产生视动性眼震。在本文中，我们描述了对称视动性眼震的发展、早期白内障剥夺对其的改变及其生理基础。然后我们提出，对于灵长类动物而言，基于通过外侧膝状体大细胞层与小细胞层的投射的解释可能比基于X、Y和W细胞的解释更为合适。
