The research described in this proposal will investigate the molecular mechanisms responsible for the development changes in the nicotinic acetylcholine receptor (nAchR) of the neuromuscular junction. The ultimate goal of this work is to understand the molecular mechanisms by which nerve changes postsynaptic properties. Specific questions that will be addressed are: 1) Are the different properties associated with adult versus embryonic receptors due to expression of different genes? 2) What role does muscle fiber electrical activity play in AchR gene expression? 3) Is adult muscle AchR gene expression localized to endplate nuclei? and 4) In what way do the subunits of the adult or embryonic AchR contribute to the different properties of these receptors? In order to investigate these questions one needs to identify the various AchR gene products expressed during development of the neuromuscular junction. Therefore, the experiments described in this proposal employ the techniques of molecular and cellular biology, muscle cell culture and recombinant DNA and antibody probes for AchR gene products.

Agency
National Institute of Health (NIH)
Institute
National Institute of Neurological Disorders and Stroke (NINDS)
Type
First Independent Research Support & Transition (FIRST) Awards (R29)
Project #
5R29NS025153-04
Application #
3477029
Study Section
Neurology C Study Section (NEUC)
Project Start
1987-07-01
Project End
1992-06-30
Budget Start
1990-07-01
Budget End
1991-06-30
Support Year
4
Fiscal Year
1990
Total Cost
Indirect Cost
Name
University of Michigan Ann Arbor
Department
Type
Schools of Medicine
DUNS #
791277940
City
Ann Arbor
State
MI
Country
United States
Zip Code
48109