Abstract
Binocular matching of orientation preference between the two eyes is a common form of binocular integration that is regarded as the basis for stereopsis. How critical period plasticity enables binocular matching under the guidance of normal visual experience has not been fully demonstrated. To investigate how critical period closure affects the binocular matching, a critical period prolonged mouse model was constructed through the administration of bumetanide, an NKCC1 transporter antagonist. Using acute in vivo extracellular recording and molecular assay, we revealed that binocular matching was transiently disrupted due to heightened plasticity after the normal critical period, together with an increase in the density of spines and synapses, and the upregulation of GluA1 expression. Diazepam (DZ)/[(R, S)-3-(2-carboxypiperazin-4-yl) propyl-1-phosphonic acid (CPP)] could reclose the extended critical period, and rescue the deficits in binocular matching. Furthermore, the extended critical period, alone, with normal visual experience is sufficient for the completion of binocular matching in amblyopic mice. Similarly, prolonging the critical period into adulthood by knocking out Nogo-66 receptor can prevent the normal maturation of binocular matching and depth perception. These results suggest that maintaining an optimal plasticity level during adolescence is most beneficial for the systemic maturation. Extending the critical period provides new clues for the maturation of binocular vision and may have critical implications for the treatment of amblyopia.
Highlights
In the visual system, an individual binocular neuron in the primary visual cortex (V1) simultaneously receives and integrates visual inputs from the two eyes
Our results showed that binocular matching was transiently postponed in bumetanide treated (Bum) mice at P35 due to heightened plasticity in a specific time window after the normal critical period, underlying that the maturation of binocular matching is dependent on the proper closure of critical period
Systemic blockade of NKCC1 co-transporter with bumetanide during the period of gamma-aminobutyric acid (GABA) depolarization (P3-P8) may transiently prolong the critical period and postpone the binocular matching, due to abnormal heightened plasticity in the visual cortex. This deficit was accompanied by changes of synaptic properties, and can be rescued by adjusting E/I balance in vivo
Summary
An individual binocular neuron in the primary visual cortex (V1) simultaneously receives and integrates visual inputs from the two eyes. Most of these V1 neurons are selective for specific stimulus orientation through each eye, and their orientation preferences are binocularly integrated in adults (Hubel and Wiesel, 1962). Amblyopia can cause many other visual impairments, such as the binocular mismatching of the orientation preference from the two eyes. There are accumulating pieces of evidence revealing that critical period plasticity is a key driver of the binocular matching process in visual cortical neurons under normal development (Wang et al, 2013; Levine et al, 2017; Mazziotti et al, 2017)
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