Lack of lateral hypothalamic orexin/hypocretin (OH) peptides (Sathiyamani et al, accompanying poster) shortens the critical period (CP) for ocular dominance plasticity (ODP) in mouse primary visual cortex (V1). We have previously shown that altered timing of the CP for ODP is caused by modified maturation of AMPA-silent synapses in both PSD-93 and PSD-95 KO mice, and results in compromised orientation discrimination (Favaro et al 2018, PLosBiol 16:e2006838). We therefore analysed whether orexin KO modifies AMPA-currents in V1 and causes similar visual deficits.First, we quantified AMPA-receptor(R), NMDAR and GABAR postsynaptic currents between L4-to-2/3 connections in acute brain slices of late CP orexin KOs. Using minimal stimulation, we observed a 50% reduction in the amplitude of AMPAR-responses, while AMPAR-silent synapse numbers remained unchanged.Second, we tested spatial vision by using both optomotry and the visual water task (VWT), a visual discrimination task. The spatial frequency threshold of the optomotor reflex was similar between WT and KO mice (WT/KO: 0.38±0.002/0.38±0.004 cyc/deg, n=5/5), suggesting that subcortical circuits mediating this reflex remain unaffected in KO mice. Using the VWT, visual acuity was reduced, but not significantly different between orexin KO and WT mice (WT/KO: 0.62±0.06/0.49±0.04 cyc/deg, n=5/5). Notably, KOs were worse in orientation discrimination, needing a larger angle difference to discriminate square wave patterns (WT/KO: 19±3°/29±3°, n=5/5, t-test p=0.035).We conclude that OH neuropeptides are required for normal visual abilities, potentially by strengthening AMPAR mediated excitation in V1.