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Abstract
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.