Developmental function of PirB restricts adult ocular dominance plasticity

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.