Grant: $100,000 - National Institutes of Health - Sep. 29, 2009
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Award Description: This research will advance new concepts in physiological and clinical translational research related to gastrointestinal motility disorders including diabetic gastroparesis. These concepts resulted from biochemical and physiological experiment dealing with cycling and regulation of the enzyme nNOS and nitrergic neurotransmission in gut. Our preliminary data using mice deficient in myosin Va and PSD95 strongly suggests loss of nitrergic neurotransmission in these mice. These results suggest that in certain disease conditions like diabetic gastroparesis, nitrergic neurotransmission is defective probably due to lack of membrane-bound nNOS. The total nNOS can still remain unaltered in these mice, as suggested in some earlier publications. However, a defect in myosin Va that can result in diminished delivery of nNOS to the membrane or deficiency of PSD95 that prevents membrane tethering of nNOS, thus resulting in impaired nitrergic neurotransmission. Impairment of nitrergic neurotransmission due to regulatory changes rather than expression of nNOS may help fully understand the patho-physiology of diabetic gastroparesis and identify new targets of therapy
Project Description: as defined in award description, above
Jobs Summary: This supplement retained the positions of 2 key personnel (1 post doc at .1 FTE and 1 faculty at .5 FTE) and a support staff at 1 FTE. The post doc participates in all criticals aspects of this proposal. A neurophysiologist who is adept in performing IJP recordings and is enormously valuable in preparing synaptosomes, running co-IP and western blotting. The retained support staff will assist project completion. and Hong Zhen He are currently being paid only part-time salaries (50%). (Total jobs reported: 0)
Project Status: Less Than 50% Completed
This award's data was last updated on Sep. 29, 2009. Help expand these official descriptions using the wiki below.