The present series of experiments was designed to study how synaptic relationships in the lateral posterior nucleus are altered after neonatal superior colliculus lesions. In this paper, we studied the lateral posterior nucleus with light and electron microscopic techniques at two critical stages: at the time of the initial neonatal tectal lesion and at the onset of the consequent proliferation of retinal axons. At birth, the lateral posterior nucleus is very immature. Very few synapses are present and no degenerating terminals were found 6 hours after a tectal lesion. Thus, very few, if any, tectal axons have established connections in the nucleus by this time and the optic tract terminals which proliferate as a result of a neonatal tectal lesion are not simply taking over vacated postsynaptic sites. Optic tract terminal proliferation begins 4 to 6 days after removal of the superior colliculus and parallels the development of the normal retinal projections to the superior colliculus and to the dorsal and ventral lateral geniculate bodies (So et al., '78). Thus, the proliferation appears to be an example of increased synapse formation during normal development rather than a case of true “axonal sprouting”. At 6 to 7 days of age, when optic tract terminal proliferation is beginning, the neuropil is still very immature. The terminal types found in the adult nucleus cannot be identified and synaptic clusters have not yet formed. Thus, following neonatal tectal lesions, the lateral posterior nucleus must undergo most of its development not only in the absence of one of its normal projections, but also in the presence of at least one anomalous projection.
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