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Critical period plasticity and sensory function in a neuroligin-3 model of autism

Extensive experience-dependent refinement of cortical circuits is restricted to critical periods of plasticity early in life. The timing of these critical periods is tightly regulated by the relative levels of excitatory and inhibitory (E/I) neurotransmission during development. Genetic disruption of synaptic proteins that normally maintain E/I balance can result in severe behavioral dysfunction in neurodevelopmental disorders like autism, but the mechanisms are unclear. We propose that abnormal critical periods of sensory circuit refinement could represent a key link between E/I imbalance and the cognitive and behavioral problems in autism. In order to test this hypothesis, we characterized visual function and the critical period for ocular dominance in the neuroligin-3-R451C mouse model of autism. This autism-associated point mutation in the postsynaptic cell adhesion molecule neuroligin-3 (R451C) has been shown to enhance cortical inhibition. We first evaluated baseline vision using in vivo electrophysiological recording in the visual cortex (V1) of anesthetized adult mice. Many properties of V1 cells were normal, including retinotopy, ocular dominance, signal-to-noise ratio, and orientation and direction selectivity. Surprisingly, visual spatial acuity was unstable throughout development and dramatically increased in young adult mutant mice when compared with wild-type littermates, indicating abnormal local circuit processing. Ocular dominance plasticity was tested over development with monocular deprivation at different ages. Plasticity was limited to the end of the first postnatal month in wild-type mice, but this