Di Stefano Marirosa, Gargini Claudia
Dipartimento di Fisiologia e Biochimica, via S. Zeno 31, 56100 Pisa, Italy.
Exp Brain Res. 2002 Nov;147(1):64-70. doi: 10.1007/s00221-002-1190-x. Epub 2002 Sep 18.
In convergent strabismus (esotropia) the spatial asynchrony of the two eye inputs unbalances the interocular interactions, leading to the functional advantage of the nondeviated eye and the inhibition of the esotropic eye. It may be argued that the strabismic suppression, if it is the effect of inhibitory interactions between the eyes, could be removed by interrupting the interocular pathways at the optic chiasm. After chiasmatic section, each eye is connected only to the ipsilateral cortex through the uncrossed retinal projections and so the functionality of each eye's input is no longer interfered with by interocular mechanisms. In strabismic cats submitted, as adults, to section of the optic chiasm, we performed electrophysiological recordings from the striate cortex. Results show that in these animals: (1) the cortical responsiveness to the strabismic eye is strikingly higher than in esotropes with an intact optic chiasm; (2) the effectiveness of stimulation of the deviated eye is not different from that of the nondeviated eye in driving neurons of corresponding cortex; (3) surprisingly, a high degree of binocular activation is present in the cortex ipsilateral to the deviated eye, while in the cortex connected to the nondeviated eye the greatest majority of neurons are monocularly driven. Cortical binocularity depends on the corpus callosum, which conveys the input from the nondeviated eye to the opposite cortex (which receives the direct strabismic input), but not vice versa. The asymmetry of callosal transmission parallels the morphological asymmetry of callosal connections that occur in convergent strabismus. All together the findings indicate that the impaired effectiveness of esotropic input does not result from developmental deficit of the strabismic afferents but, rather, from inhibitory influences that are actively exerted through the interocular pathways. Strabismic suppression may be accomplished by the same interocular mechanisms underlying binocular rivalry.
在共同性斜视(内斜视)中,双眼输入的空间不同步会使眼间相互作用失衡,导致非斜视眼具有功能优势,而斜视眼受到抑制。可以认为,如果斜视性抑制是双眼间抑制性相互作用的结果,那么通过在视交叉处中断眼间通路,这种抑制作用可能会被消除。视交叉切断术后,每只眼睛仅通过未交叉的视网膜投射与同侧皮质相连,因此每只眼睛输入的功能不再受眼间机制的干扰。对于成年后接受视交叉切断术的斜视猫,我们对其纹状皮质进行了电生理记录。结果表明,在这些动物中:(1)皮质对斜视眼的反应性明显高于视交叉完整的内斜视动物;(2)刺激斜视眼在驱动相应皮质神经元方面的有效性与刺激非斜视眼并无差异;(3)令人惊讶的是,在斜视眼同侧的皮质中存在高度的双眼激活,而在与非斜视眼相连的皮质中,绝大多数神经元是单眼驱动的。皮质双眼性依赖于胼胝体,胼胝体将来自非斜视眼的输入传递到对侧皮质(该皮质接收直接的斜视输入),反之则不然。胼胝体传递的不对称与共同性斜视中胼胝体连接的形态不对称相似。所有这些发现表明,斜视输入有效性受损并非源于斜视传入神经的发育缺陷,而是源于通过眼间通路积极发挥作用的抑制性影响。斜视性抑制可能是由双眼竞争背后的相同眼间机制完成的。