Huang L, Pallas S L
Graduate Program in Neurobiology and Behavior, Department of Biology, Georgia State University, 24 Peachtree Center Ave., Atlanta, GA 30303, USA.
J Neurophysiol. 2001 Sep;86(3):1179-94. doi: 10.1152/jn.2001.86.3.1179.
Partial ablation of the superior colliculus (SC) at birth in hamsters compresses the retinocollicular map, increasing the amount of visual field represented at each SC location. Receptive field sizes of single SC neurons are maintained, however, preserving receptive field properties in the prelesion condition. The mechanism that allows single SC neurons to restrict the number of convergent retinal inputs and thus compensate for induced brain damage is unknown. In this study, we examined the role of N-methyl-D-aspartate (NMDA) receptors in controlling retinocollicular convergence. We found that chronic 2-amino-5-phosphonovaleric acid (APV) blockade of NMDA receptors from birth in normal hamsters resulted in enlarged single-unit receptive fields in SC neurons from normal maps and further enlargement in lesioned animals with compressed maps. The effect was linearly related to lesion size. These results suggest that NMDA receptors are necessary to control afferent/target convergence in the normal SC and to compensate for excess retinal afferents in lesioned animals. Despite the alteration in receptive field size in the APV-treated animals, a complete visual map was present in both normal and lesioned hamsters. Visual responsiveness in the treated SC was normal; thus the loss of compensatory plasticity was not due to reduced visual responsiveness. Our results argue that NMDA receptors are essential for map refinement, construction of receptive fields, and compensation for damage but not overall map compression. The results are consistent with a role for the NMDA receptor as a coincidence detector with a threshold, providing visual neurons with the ability to calculate the amount of visual space represented by competing retinal inputs through the absolute amount of coincidence in their firing patterns. This mechanism of population matching is likely to be of general importance during nervous system development.
仓鼠出生时对上丘（SC）进行部分切除会压缩视网膜-上丘图谱，增加每个上丘位置所代表的视野范围。然而，单个上丘神经元的感受野大小得以维持，保留了损伤前状态下的感受野特性。单个上丘神经元限制汇聚视网膜输入数量从而补偿诱发脑损伤的机制尚不清楚。在本研究中，我们研究了N-甲基-D-天冬氨酸（NMDA）受体在控制视网膜-上丘汇聚中的作用。我们发现，从出生起对正常仓鼠的NMDA受体进行慢性2-氨基-5-磷酸缬氨酸（APV）阻断，会导致正常图谱中SC神经元的单单位感受野增大，而在图谱压缩的损伤动物中进一步增大。这种效应与损伤大小呈线性相关。这些结果表明，NMDA受体对于控制正常上丘中的传入/靶标汇聚以及补偿损伤动物中过多的视网膜传入是必要的。尽管经APV处理的动物感受野大小发生了改变，但正常和损伤的仓鼠中都存在完整的视觉图谱。处理后的上丘中的视觉反应性正常；因此，补偿性可塑性的丧失并非由于视觉反应性降低。我们的结果表明，NMDA受体对于图谱细化、感受野构建和损伤补偿至关重要，但对于整体图谱压缩并非如此。这些结果与NMDA受体作为具有阈值的巧合探测器的作用一致，使视觉神经元能够通过其放电模式中的绝对巧合量来计算由相互竞争的视网膜输入所代表的视觉空间量。这种群体匹配机制在神经系统发育过程中可能具有普遍重要性。
