Article Cortical feedback modulates distinct critical period development in mouse visual thalamus

In primary visual cortex (V1), critical period for ocular dominance (OD) plasticity is a well-defined developmental stage to shape neuronal circuits based on visual experience. Recent studies showed that V1-like OD plasticity existed in mouse dorsal lateral geniculate nucleus (dLGN). It is still unclear what the exact time win-dow is and how neural circuits contribute to OD plasticity in dLGN. Using in vivo electrophysiology, we defined a critical period for OD plasticity in dLGN from eye opening to puberty. There also existed an innate process of OD formation from contralateral to equal bias in dLGN binocular neurons. Instant V1 inactivation with muscimol had no effect on OD bias or plasticity. Short-term V1 inactivation with N-methyl-d-aspartate reversed the formation of equal OD bias, while long-term V1 inactivation retained dLGN development to an immature stage.

Automated summary

In mouse dorsal lateral geniculate nucleus (dLGN), a critical period for ocular dominance (OD) plasticity has been identified from eye opening to puberty. There is an innate process of OD formation from contralateral to equal bias in dLGN binocular neurons. Inactivation of primary visual cortex (V1) has different effects on OD bias and plasticity in dLGN, with short-term inactivation reversing the formation of equal OD bias and long-term inactivation retaining dLGN development to an immature stage.