Compromised binocular vision and reduced binocularity in the visual cortex of postsynaptic density 95 (PSD-95) knock-out mice

Postsynaptic density protein 95 (PSD-95) is an important signalling scaffold of the PSD of excitatory synapses. We have previously shown that PSD-95 dependent silent synapse maturation closes the critical period (CP) for ocular dominance plasticity in mouse V1: PSD-95 KO mice display both functional & structural hallmarks of CP plasticity and synapses cannot properly stabilize. Since the development of binocularity happens during the CP, we hypothesized that PSD-95 KOs should display compromised binocular integration. To test this hypothesis, we performed both behavioural experiments and multi-electrode electrophysiological recordings in primary visual cortex (V1) of awake mice. In fact, PSD-95 KO mice are better in an orientation discrimination task (visual water task) under monocular compared to binocular conditions, unlike WT, who get worse. PSD-95 KOs are also worse compared to WT in catching crickets, a behaviourally relevant visual task, shown to exploit binocular vision. Furthermore, PSD-95 KOs improve in prey capture with monocular vision, unlike WT-mice. Finally, our electrophysiolgical data show that V1 of awake PSD-95 KO – compared to WT-mice – hosts fewer binocular orientation selective units and binocular responses are dominated by contralateral eye inputs, indicative of disturbed binocular interactions. In addition, PSD-95 KOs display less binocular facilitation/summation and reduced direction selectivity. Since direction selectivity requires early visual experience this can likely be explained by the non-stabilized V1-synapses of PSD-95 KOs. Together, our data strongly support a role of experience-dependent silent synapse maturation for the refinement of cortical circuitry for proper binocular signal processing and vision. Supported by CRC889