An important feature of visual cortex development is that during early postnatal life neurons in the visual cortex are susceptible to activity-dependent modifications. Visual experience can dramatically alter responses of visual cortical neurons. This experience-dependent plasticity, however, occurs only within a critical period during early postnatal development. The same visual experience that can cause dramatic changes in developing visual cortex is no longer effective to induce changes in adult visual cortex. Although differential gene expression has been proposed as a basis of the critical period, the molecular nature of the critical period remains elusive. Several laboratories have been utilizing molecular biological techniques such as cDNA micoarray, differential display, and subtractive hybridization to identify candidate molecules that may play a key role in visual cortex development and plasticity. Most of the studies, however, have been focused on gene expression at the mRNA level, with the assumption that the relative mRNA levels represent the relative levels of proteins. However, evidence is available including from visual cortex suggesting that the levels of mRNAs and proteins often do not correlate. Therefore, it becomes more important to examine gene expression at the protein level than at the mRNA level. The objective of this proposal is to examine changes of protein expressions in the visual cortex during postnatal development using a new emerging technique, antibody microarray, which is a powerful chip-based technology for profiling hundreds of proteins simultaneously. This proposal consists of two specific aims: 1. To examine relative expression levels of over 500 proteins in the primary visual cortex during postnatal development. 2. To identify, among these proteins, candidate molecules that may play an important role in visual cortex plasticity. Visual cortex plasticity is the neural basis for certain visual disorders such as amblyopia and strabismus which together afflict more than five million North Americans. Understanding molecular mechanisms of visual cortex plasticity will help developing effective therapeutic approaches to treat adult amblyopia and strabismus.

Agency
National Institute of Health (NIH)
Institute
National Eye Institute (NEI)
Type
Small Research Grants (R03)
Project #
5R03EY014892-02
Application #
6908873
Study Section
Special Emphasis Panel (ZEY1-VSN (01))
Program Officer
Oberdorfer, Michael
Project Start
2004-07-01
Project End
2007-05-31
Budget Start
2005-06-01
Budget End
2006-05-31
Support Year
2
Fiscal Year
2005
Total Cost
$143,500
Indirect Cost
Name
Wake Forest University Health Sciences
Department
Anatomy/Cell Biology
Type
Schools of Medicine
DUNS #
937727907
City
Winston-Salem
State
NC
Country
United States
Zip Code
27157
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Gu, Qiang; Sivanandam, Thamil Mani; Kim, Caroline Aehyun (2006) Signal stability of Cy3 and Cy5 on antibody microarrays. Proteome Sci 4:21
Li, P; Prasad, S S; Mitchell, D E et al. (2006) Postnatal expression profile of OBCAM implies its involvement in visual cortex development and plasticity. Cereb Cortex 16:291-9