Long-term Monocular Deprivation during Juvenile Critical Period Disrupts Binocular Integration in Mouse Visual Thalamus

• DOI: 10.1523/jneurosci.1626-19.2019
• Publication Date: 2019-11-25T22:49:18Z
• Authors: Carey Y.L. Huh; Karim Abdelaal; Kirstie J. Salinas; Diyue Gu; Jack Zeitoun; Dario X. Figueroa...; John P. Peach; Charless C. Fowlkes; Sunil P. Gandhi
• Keywords: Monocular deprivation; Monocular; Lateral geniculate nucleus; Ocular dominance column; Sensory deprivation

Study of the neural deficits caused by mismatched binocular vision in early childhood has predominantly focused on circuits primary visual cortex (V1). Recent evidence revealed that neurons mouse dorsolateral geniculate nucleus (dLGN) can undergo rapid ocular dominance plasticity following monocular deprivation (MD). It remains unclear, however, whether long-lasting attributed to MD during critical period originate thalamus. Using vivo two-photon Ca 2+ imaging dLGN afferents superficial layers V1 female and male mice, we demonstrate 14 d leads a chronic loss inputs while sparing response strength spatial acuity. Importantly, profoundly tuning properties remaining afferents. Furthermore, impairs modulation, reducing facilitation responses both viewing. As predicted our findings thalamic inputs, from spared acuity but impaired binocularity L4 neurons. L2/3 contrast displayed Our data critical-period produces disruptions integration beginning dLGN, whereas first arise further downstream V1. indicate development normal depend upon experience-dependent refinement distinct stages mammalian system. SIGNIFICANCE STATEMENT Abnormal reduced are hallmarks amblyopia, disorder affects 2%–5% population. is widely thought underlying amblyopia begin cortex. calcium thalamocortical axons show depriving one eye input chronically In contrast, inputs. These shed new light role for developmental mechanisms thalamus establishing may have implications amblyopia.