Genetic control of experience-dependent plasticity in the visual cortex.

Area of Science:

• Neuroscience
• Genetics
• Developmental Biology

Background:

• Monocular deprivation during development alters ocular dominance (OD) in the primary visual cortex (V1).
• Understanding the genetic basis of this cortical plasticity is crucial for developmental neuroscience.
• Recombinant inbred mouse strains offer a powerful model for studying the heritability of complex traits.

Purpose of the Study:

• To determine the heritability of ocular dominance plasticity in response to monocular deprivation.
• To identify specific gene loci associated with variations in OD plasticity.
• To investigate potential candidate genes, such as Stch and Nrip1, involved in visual cortex development.

Main Methods:

• Utilized a large cohort of BXD recombinant inbred mouse strains derived from C57BL/6J and DBA/2J backgrounds.
• Assessed ocular dominance plasticity by measuring intrinsic signal responses in V1 following monocular visual deprivation.
• Employed quantitative trait locus (QTL) mapping to identify genetic regions influencing OD plasticity.

Main Results:

• Ocular dominance plasticity and the strength of V1 responses to visual stimuli demonstrated significant heritability across BXD strains.
• Observed considerable variation in OD plasticity among different BXD strains, with C57BL/6J showing the most pronounced shift.
• Identified a QTL regulating the response change in the deprived eye, encompassing 13 genes, including Stch and Nrip1, which harbor missense polymorphisms.

Conclusions:

• Ocular dominance plasticity exhibits substantial genetic control, with significant implications for using genetically diverse mouse models.
• The distinct genetic regulation of ipsilateral and contralateral eye responses suggests complex underlying mechanisms.
• Stch and Nrip1 are identified as novel candidate genes for ocular dominance plasticity based on expression correlation and polymorphisms.