Intrauterine enucleation of normal mice mimics a structural compensatory response in the geniculate of eyeless mutant mice.

Identification of a compensatory structural pathway for the retinal terminals in the glomerular configuration of the dorsal lateral geniculate nucleus (dLGN) of the adult anophthalmic mutant mouse (ZRDCT-An) led to an experimental analysis of the effect of surgical enucleation on the dLGN of normal embryonic and postnatal C57 mice. Young C57 adults were prenatally enucleated (embryonic days 14-19) or during the early postnatal period (birth to 5 days old). Light and electron microscopic observations on the dLGN of these enucleated mice were compared with the dLGN of two types of mutant mice, the bilaterally eyeless anophthalmic and the unilaterally eyeless naked splotch (NSP). A structural compensatory response, similar to that occurring naturally in these two mutant mice, is activated by prenatal experimental enucleation as shown by the appearance of large replacement terminals (LRTs) for the retinal afferents. The glomeruli in the ipsi- and/or contralateral dLGN in these 3 conditions contain extensive synaptic areas covered by compensatory large axons. This pattern of synaptic thalamic reorganization occurs after experimental prenatal and postnatal enucleation of normal mice. This structural reorganization in experimentally and genetically enucleated mice suggests a common mechanism for replacement of retinal terminals. The precise origin and function of this tract remains to be determined. This evidence demonstrates that the anophthalmic mutant mouse is a valid model system for analysis of thalamic reorganization that occurs in normal mice after perinatal enucleation.