Genetic control of experience-dependent plasticity in the visual cortex
Article first published online: 12 AUG 2008
DOI: 10.1111/j.1601-183X.2008.00431.x
© 2008 The Authors Journal compilation © 2008 Blackwell Publishing Ltd/International Behavioural and Neural Genetic Society
Additional Information
How to Cite
Heimel, J. A., Hermans, J. M., Sommeijer, J.-P., Neuro-Bsik Mouse Phenomics consortium and Levelt, C.N. (2008), Genetic control of experience-dependent plasticity in the visual cortex. Genes, Brain and Behavior, 7: 915–923. doi: 10.1111/j.1601-183X.2008.00431.x
Publication History
- Issue published online: 24 NOV 2008
- Article first published online: 12 AUG 2008
- Received 8 April 2008, revised 1 July 2008, accepted for publication 3 August 2008
Keywords:
- BXD;
- down syndrome;
- Nrip1;
- ocular dominance;
- quantitative trait loci;
- recombinant inbred;
- Stch
Depriving one eye of visual experience during a sensitive period of development results in a shift in ocular dominance (OD) in the primary visual cortex (V1). To assess the heritability of this form of cortical plasticity and identify the responsible gene loci, we studied the influence of monocular deprivation on OD in a large number of recombinant inbred mouse strains derived from mixed C57BL/6J and DBA/2J backgrounds (BXD). The strength of imaged intrinsic signal responses in V1 to visual stimuli was strongly heritable as were various elements of OD plasticity. This has important implications for the use of mice of mixed genetic backgrounds for studying OD plasticity. C57BL/6J showed the most significant shift in OD, while some BXD strains did not show any shift at all. Interestingly, the increase in undeprived ipsilateral eye responses was not correlated to the decrease in deprived contralateral eye responses, suggesting that the size of these components of OD plasticity are not genetically controlled by only a single mechanism. We identified a quantitative trait locus regulating the change in response to the deprived eye. The locus encompasses 13 genes, two of which –Stch and Nrip1 – contain missense polymorphisms. The expression levels of Stch and to a lesser extent Nrip1 in whole brain correlate with the trait identifying them as novel candidate plasticity genes.
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