NMDA antagonists in the superior colliculus prevent developmental plasticity but not visual transmission or map compression

Partial ablation of the superior colliculus (SC) at birth in hamsters compr esses the retinocollicular map, increasing the amount of visual field repre sented 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 num ber of convergent retinal inputs and thus compensate for induced brain dama ge 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 f rom birth in normal hamsters resulted in enlarged single-unit receptive fie lds in SC neurons from normal maps and further enlargement in lesioned anim als with compressed maps. The effect was linearly related to lesion size. T hese results suggest that NMDA receptors are necessary to control afferent/ target convergence in the normal SC and to compensate for excess retinal af ferents in lesioned animals. Despite the alteration in receptive field size in the APV-treated animals, a complete visual map was present in both norm al and lesioned hamsters. Visual responsiveness in the treated SC was norma l; thus the loss of compensatory plasticity was not due to reduced visual r esponsiveness. Our results argue that NMDA receptors are essential for map refinement, construction of receptive fields, and compensation for damage b ut not overall map compression. The results are consistent with a role for the NMDA receptor as a coincidence detector with a threshold, providing vis ual neurons with the ability to calculate the amount of visual space repres ented by competing retinal inputs through the absolute amount of coincidenc e in their firing patterns. This mechanism of population matching is likely to be of general importance during nervous system development.