| Summary: | Ocular dominance plasticity (ODP) is a well-characterized example of experience-dependent
plasticity. Multiple molecular mechanisms have been implicated in the studying of ODP. We
have previously demonstrated a temporal correlation between long-term depression (LTD) and
ocular dominance plasticity. It has also been shown that blockade of LTD abolishes ocular
dominance shift during the critical period, suggesting that LTD is necessary for ocular
dominance plasticity. Here I go on to explore if LTD is sufficient for ocular dominance plasticity
by augmenting it in adulthood. By administering D-serine, an NMDAR co-agonist that
selectively enhances LTD in adult visual cortex, I am able to enhance ocular dominance
plasticity in adulthood, as evidenced by data collected from single-unit recordings. D-serine
operates via an LTD-like mechanism as its effect could be abolished by GluR23Y peptide, a
selective LTD blocker. I therefore argue that LTD plays a key regulatory role in both juvenile
and adult ocular dominance plasticity. In addition, D-serine helps facilitate recovery of visual
input in long-term monocularly deprived adult mice, suggestive of therapeutic potentials.
In addition, I have examined the functional consequences of monocular deprivation on
the rest of primary visual cortex (V1) and cerebral cortex. This is achieved with help of in vivo imaging of intrinsic optic signals and calcium imaging. Within the visual cortex, monocular
deprivation decreases the correlation between the contralateral monocular zone with the rest of
V1. I have also observed transient changes in global functional connectivity correlating with the
duration of lid suture during the critical period, in keeping with cross-modal plasticity. However,
this change in functional connectivity is not observed in adulthood, suggesting a sensory period
for cross-modal connectivity. === Medicine, Faculty of === Graduate
|
|---|
