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Ultrastructural development of the dorsal lateral geniculate nucleus of genetically microphthalmic mice
Abstract:
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.
Insights
Microphthalmic mice (mi/mi) lack typical retinal axon terminals in the dorsal lateral geniculate nucleus (dLGN). These are replaced by abnormal large boutons, suggesting developmental defects in visual pathway formation.
Area of Science:
- Neuroscience
- Developmental Biology
- Ophthalmology
Background:
- The dorsal lateral geniculate nucleus (dLGN) is a key structure in the visual pathway.
- Microphthalmia is a congenital disorder characterized by small eyes.
- Understanding visual pathway development in genetic disorders is crucial.
Purpose of the Study:
- To investigate the ultrastructure of the dLGN in microphthalmic mice (mi/mi).
- To characterize the types and origins of axon terminals in the dLGN of affected and normal littermates.
Main Methods:
- Electron microscopy was used to examine the dLGN ultrastructure.
- Axon terminal populations were identified and characterized based on vesicle morphology and mitochondrial appearance.
- Eye enucleation was performed to assess terminal degeneration and infer origin.
Main Results:
- Microphthalmic mice (mi/mi) lack typical retinal endings (RLP) in the dLGN.
- These are replaced by large boutons with round vesicles and dark mitochondria (RLD), which do not degenerate after enucleation.
- Normal littermates possess RLP terminals that degenerate after enucleation, alongside non-degenerate RLD terminals of unclear origin.
Conclusions:
- The RLD terminals in mi/mi mice are not of retinal origin and represent a replacement phenomenon.
- The findings suggest abnormal developmental processes in the visual thalamus of microphthalmic mice.
- The origin of RLD terminals requires further investigation, potentially implicating non-cortical pathways.