Randomized Retinal Ganglion Cell Axon Routing at the Optic Chiasm of GAP-43-Deficient Mice: Association with Midline Recrossing and Lack of Normal Ipsilateral Axon Turning
| Autor: | Kelly Kruger, David W. Sretavan |
|---|---|
| Rok vydání: | 1998 |
| Předmět: |
Retinal Ganglion Cells
genetic structures Optic tract Population Optic chiasm Biology Article Functional Laterality Retina Mice GAP-43 Protein medicine Animals Telodendron Axon education Mice Knockout education.field_of_study General Neuroscience Cell Differentiation Anatomy Embryo Mammalian Axons eye diseases medicine.anatomical_structure nervous system Retinal ganglion cell Optic Chiasm Axon guidance sense organs Neuroscience |
| Zdroj: | The Journal of Neuroscience. 18:10502-10513 |
| ISSN: | 1529-2401 0270-6474 |
| DOI: | 10.1523/jneurosci.18-24-10502.1998 |
| Popis: | During mammalian development, retinal ganglion cell (RGC) axons from nasal retina cross the optic chiasm midline, whereas temporal retina axons do not and grow ipsilaterally, resulting in a projection of part of the visual world onto one side of the brain while the remaining part is represented on the opposite side. Previous studies have shown that RGC axons in GAP-43-deficient mice initially fail to grow from the optic chiasm to form optic tracts and are delayed temporarily in the midline region. Here we show that this delayed RGC axon exit from the chiasm is characterized by abnormal randomized axon routing into the ipsilateral and contralateral optic tracts, leading to duplicated representations of the visual world in both sides of the brain. Within the chiasm, individual contralaterally projecting axons grow in unusual semicircular trajectories, and the normal ipsilateral turning of ventral temporal axons is absent. These effects on both axon populations suggest that GAP-43 does not mediate pathfinding specifically for one or the other axon population but is more consistent with a model in which the initial pathfinding defect at the chiasm/tract transition zone leads to axons backing up into the chiasm, resulting in circular trajectories and eventual random axon exit into one or the other optic tract. Unusual RGC axon trajectories include chiasm midline recrossing similar to abnormal CNS midline recrossing in invertebrate “roundabout” mutants andDrosophilawith altered calmodulin function. This resemblance and the fact that GAP-43 also has been proposed to regulate calmodulin availability raise the possibility that calmodulin function is involved in CNS midline axon guidance in both vertebrates and invertebrates. |
| Databáze: | OpenAIRE |
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