Abstract: PURPOSE: Long-term monocular visual deprivation (MD) during early life causes visual acuity deficiency (amblyopia) and a progressive loss of neuronal responsiveness and selectivity in the primary visual cortex (V1) through the deprived eye, such as ocular dominance and orientation selectivity. Recent studies about experience-dependent plasticity in the visual cortex show that visual perceptual learning seems to be a therapeutic strategy for recovery in older children and adults with amblyopia and the neural circuit plasticity maybe a potential explanation. To explore the neural mechanisms underlying visual training, we investigated the effects of binocular visual training on the visual responses of neurons in V1 and vision recovery from early-onset, long-term MD.
METHODS: We used optomotor response to measure the visual acuity threshold of an amblyopic model of mice to assess vision recovery from early-onset, long-term MD with or without a brief period of binocular visual training. We also employed two-photon calcium imaging and chemogenetic technique to investigate the visual responses (i.e., ODI and OSI) of individual excitatory neuron and parvalbumin-positive (PV) interneuron in V1.
RESULTS: We found that binocular visual training promoted visual acuity threshold, activated the response of excitatory neurons but decreased the response of PV interneurons in V1 of adult amblyopia mice. Moreover, activation of PV interneurons offset the vision-promoting effects of visual training and disinhibition of PV interneurons enhanced the vision-promoting effects of visual training.
CONCLUSIONS: We found that binocular visual training decreased the response of PV interneuron, resulting in an attenuation of inhibition onto excitatory neurons and sustained cortical disinhibition to enhance cortical plasticity in adult visual cortex. Our results demonstrate the neural plasticity-based mechanism for visual stimulation-mediated functional recovery from adult amblyopia.

Key words: visual training, visual cortex plasticity, amblyopia, neuron.