Gingras Guy, Mitchell Donald E, Hess Robert F
Psychology Department, Dalhousie University, Halifax Nova Scotia, B3H 4J1, Canada.
Eur J Neurosci. 2005 Jul;22(1):119-24. doi: 10.1111/j.1460-9568.2005.04201.x.
Identification of the neural basis of the visual deficits experienced by humans with amblyopia, particularly when associated with strabismus (strabismic amblyopia), has proved to be difficult in part because of the inability to observe directly the neural changes at various levels of the human visual pathway. Much of our knowledge has necessarily been obtained on the basis of sophisticated psychophysical studies as well as from electrophysiological explorations on the visual pathways in animal models of amblyopia. This study combines these two approaches to the problem by employing similar psychophysical probes of performance on animal models of two forms of amblyopia (deprivation and strabismic) to those employed earlier on human amblyopes (Hess & Field, 1994, Vis. Res., 34, 13397-13406). The tests explore two competing explanations for the visual deficits, namely an evenly distributed loss of neural connections (undersampling) with the amblyopic eye as opposed to disordered connections with this eye (neural disarray). Unexpectedly, the results in animal models of deprivation amblyopia were not in accord with expectations based upon an even distribution of lost connections with the amblyopic eye. However, the results were similar to those observed in a strabismic amblyopic animal and to strabismic amblyopic humans. We suggest that deprivation amblyopia may be accompanied by an uneven loss of connections that results in effective neural disarray. By contrast, amblyopia associated with strabismus might arise from neural disarray of a different origin such as an alteration of intrinsic cortical connections.
事实证明，确定患有弱视的人，尤其是伴有斜视（斜视性弱视）的人所经历的视觉缺陷的神经基础很困难，部分原因是无法直接观察人类视觉通路各个层面的神经变化。我们的许多知识必然是基于复杂的心理物理学研究以及对弱视动物模型视觉通路的电生理探索而获得的。本研究通过对两种弱视（剥夺性和斜视性）动物模型采用与早期对人类弱视患者所采用的类似心理物理学性能探测方法（Hess & Field，1994，《视觉研究》，34，13397 - 13406），将这两种解决该问题的方法结合起来。这些测试探究了对视觉缺陷的两种相互竞争的解释，即弱视眼神经连接均匀分布的丧失（欠采样）与该眼连接紊乱（神经紊乱）。出乎意料的是，剥夺性弱视动物模型的结果与基于弱视眼连接均匀丧失的预期不符。然而，这些结果与在斜视性弱视动物以及斜视性弱视人类中观察到的结果相似。我们认为，剥夺性弱视可能伴随着连接的不均匀丧失，从而导致有效的神经紊乱。相比之下，与斜视相关的弱视可能源于不同起源的神经紊乱，例如内在皮质连接的改变。
