UC San Diego
Molecular and cellular mechanisms of retinotopic mapping in the superior colliculus
- Author(s): Bevins, Nicholas James
- et al.
Retinal ganglion cells (RGCs) project axons from their cell bodies in the eye to targets in the superior colliculus (SC) of the midbrain. The wiring of RGC axons to their synaptic targets creates an ordered representation, or ̀map', of retinal space within the brain. The mechanisms of development of this map are the primary topic of this dissertation. The dissertation begins with an overview of the architecture and function of the murine visual system with a focus on RGCs. The paradigms of retinotopic map development have been divided into those involving guidance molecules and those involving correlated activity. I describe a set of ratiometric 'Relative Signaling' (RS) rules that quantitatively predict how a composite gradient of EphA receptors expressed by RGCs is translated into topographic order in the SC. I describe the analysis of the retinotopic maps of novel compound mutant mice, which establish the general utility of the RS rules for predicting retinocollicular topography, including the equivalence of different EphA receptor gene products. I describe how spontaneous, patterned activity in the retina during the time of retinocollicular mapping could be instructive to the development of retinotopy. I analyze the retinocollicular maps of novel compound mutant mice lacking the [beta]2 subunit of the nicotinic acetylcholine receptor, which are thought to lack spontaneous, patterned activity in the retina. The analysis of retinocollicular maps in these compound mutant mice was ambiguous, but suggested that correlated activity does not play a role in retinocollicular mapping. Finally, I speculate on how different dynamics of retinotopic mapping in amniotes and anamniotes may arise because of the differing degree of encephalization between the two groups. I also comment on how increased encephalization allows for a greater behavioral repertoire but comes at the costs of an inability to regenerate and a greater time to develop