Genetic dissection of the critical period for plasticity in mouse visual cortex


July 9, 2014 - 1:00pm
NW 243
About the Speaker
Aaron Mcgee (USC)

Why does discordant vision only during a childhood ‘critical period’ induce amblyopia (lazy-eye)? Why does this disorder cause enduring visual impairment even if the underlying causes are corrected in adulthood? This is in part because experience-dependent plasticity is limited in the maturing brain by factors present in the neuropil, including myelination and extracellular matrix. Several of these inhibitory factors signal through the neuronal Nogo receptor (NgR1). The ngr1 gene is required to close a ‘critical period’ for visual plasticity and mice lacking this gene spontaneously recover normal visual acuity in a rodent model of amblyopia. We are investigating how NgR1 restricts visual plasticity with a combination of conditional mouse genetics, electrophysiology, chronic in vivo imaging, and behavioral assays. In parallel experiments, we are exploring how NgR1 may constrain related forms of adult plasticity, such as perceptual learning. NgR1 mutant mice exhibit greater improvement and better overall performance in the gap crossing (GC) learning paradigm although basal turnover of dendritic spines and axonal boutons in vivo are normal. Thus, ngr1 appears to serve as a brake on sensory plasticity but does appear to function by determining the low set point for synaptic turnover in the associated sensory cortex.