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Mann, Miriam (2009): Developmental function of PirB restricts adult ocular dominance plasticity. Dissertation, LMU München: Fakultät für Biologie



Early visual input induces changes in functional connectivity which can either lead to the stabilisation of appropriate synaptic connections or the elimination of inappropriate ones in the visual system. Monocular deprivation (MD) is a widely used paradigm to study changes in ocular dominance (OD) in the binocular visual cortex of higher mammals. Closure of one eye for several days leads to a shift in OD which re ects changes in the response kinetics of the deprived and the non-deprived eye. The molecular machinery which underlies this type of experience-dependent plasticity is still elusive. A recent genetic screen in the lab of Carla Shatz has identied that the family of MHCI receptors are expressed in the developing visual cortex and regulated upon neuronal activity. They hypothesized that MHC receptors might be required for consolidation of longlasting changes in synaptic strength. To investigate the role of MHCI in OD plasticity, I used a transgenic mouse lacking the MHCI receptor paired-immunoglobulin-like receptor B (PirB). To determine OD in the mouse visual cortex, I used optical imaging of intrinsic signals which measures the activity of neuronal populations elicited from either eye stimulation. Beforehand I investigated OD plasticity in adult mice (C57Bl6) which is still questioned to be present after MD. I conrmed earlier ndings which have shown robust MD induced changes of either eye in the visual cortex of adult mice. In the next chapter I explored eye specic kinetics during the critical period (postnatal days (P)19-32) in PirB KO mice. Closed eye depression occurred more rapidly and was stronger in KO mice in comparison to WT mice. I was also interested whether the mechanisms of OD plasticity in adult PirB KO (P90) mice diered from that juvenile PirB KO mice. Interestingly I observed a tendency for similar eye specic kinetics in adult PirB KO mice and in juvenile WT mice, which lead to the speculation that removal of PirB might reinduce juvenile like plasticity in adult mice. A recent study in the lab investigated the effect of prior experience and could show that OD plasticity in adult mice was enhanced due to an inital MD in juvenile mice and a subsequent MD of the same eye in adulthood. Would PirB play a role in this type of enhanced plasticity? Surprisingly I explored that OD plasticity in PirB KO mice is the same after a single or repeated exposure to MD, suggesting that the capacity for plasticity in these mice is near saturation. In the last chapter I addressed the question whether the representation of both eyes in the binocular visual cortex is dierent in PirB KO mice in comparison to WT mice. Therefore I showed stimuli in the central and peripheral visual field of adult non-deprived and deprived PirB KO mice. I found enhanced response strength in the open eye after peripheral visual eld stimulation in deprived PirB KO mice in contrast to WT mice. Overall I assessed stronger and more rapid functional plasticity in PirB KO mice during development and adulthood. Hence I postulate that PirB might act as a molecular brake limiting OD plasticity.