An interdepartmental group of NIH-supported investigators seeks funds for a Perkin-Elmer Wallac Ultraview confocal microscope system, to replace and upgrade an existing Noran system that has several major deficiencies and is starting to fail. The requested system has several important advantages that will benefit many NIH-sponsored research programs at this institution. The noel design of this confocal system allows use of very low intensities of excitation light, thus minimizing phototoxicity and bleaching. The high sensitivity of the light-detection systems permits measurements of weaker signals than can be detected by our current confocal system. The requested system also has a much better data-collecting ability (14 bit sampling) than the existing system (8 bits). The application details why the requested confocal system is essential and/or important for optimal progress of NIH-sponsored projects of major users from five laboratories. Four of the laboratories will be imaging living tissues, and share research interests in mitochondrial function. All major users have a history of cooperative interactions, and one has access to any other suitable confocal facility. The confocal needs of five additional laboratories are briefly summarized. All major users attended a demonstration of the requested confocal system at the University of Miami, during which some of the tissues and fluorophores to be imaged were examined. In all cases the requested confocal system, facilitating experiments that are now difficult or impossible to perform.
| Talbot, Janet D; Barrett, John N; Barrett, Ellen F et al. (2008) Rapid, stimulation-induced reduction of C12-resorufin in motor nerve terminals: linkage to mitochondrial metabolism. J Neurochem 105:807-19 |
| Talbot, Janet; Barrett, John N; Barrett, Ellen F et al. (2007) Stimulation-induced changes in NADH fluorescence and mitochondrial membrane potential in lizard motor nerve terminals. J Physiol 579:783-98 |
| David, Gavriel; Nguyen, Khanh; Barrett, Ellen F (2007) Early vulnerability to ischemia/reperfusion injury in motor terminals innervating fast muscles of SOD1-G93A mice. Exp Neurol 204:411-20 |
| Garcia-Chacon, Luis E; Nguyen, Khanh T; David, Gavriel et al. (2006) Extrusion of Ca2+ from mouse motor terminal mitochondria via a Na+-Ca2+ exchanger increases post-tetanic evoked release. J Physiol 574:663-75 |
