Ultrastructural development of the dorsal lateral geniculate nucleus of genetically microphthalmic mice.
The ultrastructure of the dorsal lateral geniculate nucleus (dLGN) of microphthalmic mice is described in affected white homozygotes (mi/mi) and their apparently normal grey littermates. In the dLGN of mi/mi animals populations of apparently normal axon terminals were observed, including some with flattened synaptic vesicles and other small terminals with round vesicles and dark mitochondria (RSD), possibly of cortico-thalamic origin, just as in normal mice. However, no typical large retinal endings with round vesicles and pale mitochondria (RLP) are visible. Instead they appear to be replaced by other large boutons with round vesicles and dark mitochondria (RLD). Eye enucleation does not cause degeneration of these RLD terminals. In apparently normal grey littermates RLP terminals are present and they degenerate when an eye is enucleated. But RLD endings are also found in these animals, and never degenerate after enucleation. The origin of the RLD terminals is unclear but seems not to be cortical. These findings are compared with those of Cullen and Kaiserman-Abramof (1976) in a different strain (ZRDCT-An) of anophthalmic mouse in which they found large replacement terminals similar to our RLD boutons.
D000818:Animals; D004195:Disease Models, Animal; D005829:Geniculate Bodies / Q000648:ultrastructure*; D051379:Mice; D008817:Mice, Mutant Strains; D008850:Microphthalmos / Q000235:genetics / Q000473:pathology* / Q000503:physiopathology; D008854:Microscopy, Electron; D009410:Nerve Degeneration; D009411:Nerve Endings / Q000648:ultrastructure; D009474:Neurons / Q000648:ultrastructure*; D012683:Sensory Deprivation