Research Topics
Genomes and GenesSpecies | Gavriel DavidSummaryAffiliation: University of Miami Country: USA Publications
Research Grants
| Collaborators
|
Detail Information
Publications
Early vulnerability to ischemia/reperfusion injury in motor terminals innervating fast muscles of SOD1-G93A miceGavriel David
Department of Physiology and Biophysics, University of Miami Miller School of Medicine, USA
Exp Neurol 204:411-20. 2007..Early vulnerability of fast motor terminals to I/R injury thus may signal, and possibly contribute to, early events involved in motor neuron death...- Inhibition of mitochondrial Ca2+ uptake affects phasic release from motor terminals differently depending on external [Ca2+]Janet D Talbot
Department of Physiology and Biophysics, University of Miami School of Medicine, Miami, Florida 33136, USA
J Neurophysiol 90:491-502. 2003..5 mM Ca2+. A similar convergence was measured in oligomycin, which inhibits mitochondrial ATP synthesis without depolarizing mitochondria, but quantal contents fell to <20 when mitochondria were depolarized in 2 mM Ca2+... - Rapid, stimulation-induced reduction of C12-resorufin in motor nerve terminals: linkage to mitochondrial metabolismJanet D Talbot
Department of Physiology and Biophysics, Miller School of Medicine, University of Miami, Miami, Florida 33101, USA
J Neurochem 105:807-19. 2008.... - Stimulation-induced changes in NADH fluorescence and mitochondrial membrane potential in lizard motor nerve terminalsJanet Talbot
Department of Physiology and Biophysics, Miller School of Medicine, University of Miami, PO Box 016430, Miami, FL 33101, USA
J Physiol 579:783-98. 2007..These results suggest that the ability to accelerate ETC activity is important for normal mitochondrial sequestration of stimulation-induced Ca2+ loads... - Quantitative estimate of mitochondrial [Ca2+] in stimulated motor nerve terminalsGavriel David
Department of Physiology and Biophysics, University of Miami School of Medicine, R 430, P O Box 016430, Miami, FL 33101, USA
Cell Calcium 33:197-206. 2003..The high K(d) of rhod-5N ensures that this value is not a result of dye saturation, but rather reflects a powerful Ca(2+) buffering mechanism within the matrix of these mitochondria... - Repetitive nerve stimulation transiently opens the mitochondrial permeability transition pore in motor nerve terminals of symptomatic mutant SOD1 miceKhanh T Nguyen
Department of Physiology and Biophysics, University of Miami Miller School of Medicine, PO Box 016430, Miami, FL 33101, USA
Neurobiol Dis 42:381-90. 2011..m) depolarizations resembling those in symptomatic fALS mice could be elicited in wild-type mice following a 0.5-1h exposure to diamide (200 ?M), which produces an oxidative stress, but these depolarizations were not reduced by CsA... - Vesicular ATPase inserted into the plasma membrane of motor terminals by exocytosis alkalinizes cytosolic pH and facilitates endocytosisZhongsheng Zhang
Department of Physiology and Biophysics, Miller School of Medicine, University of Miami, Miami, FL 33136, USA
Neuron 68:1097-108. 2010..The resulting cytosolic alkalinization may facilitate vesicular endocytosis... - Calcium dependence of damage to mouse motor nerve terminals following oxygen/glucose deprivationJanet D Talbot
Department of Physiology and Biophysics, University of Miami Miller School of Medicine, P O Box 016430, Miami, FL 33101, USA
Exp Neurol 234:95-104. 2012..There was no significant difference between the response of wild-type and presymptomatic superoxide dismutase 1 G93A mutant terminals to OGD, or in their response to the protective effect of the tested drugs... - Mitochondria in motor nerve terminals: function in health and in mutant superoxide dismutase 1 mouse models of familial ALSEllen F Barrett
Department of Physiology and Biophysics, R 430, University of Miami Miller School of Medicine, Miami, FL 33136, USA
J Bioenerg Biomembr 43:581-6. 2011..This dysfunction would impair mitochondrial ability to sequester stimulation-associated Ca(2+) loads, and thus likely contributes to the early degeneration of motor terminals... - Mitochondrial Ca2+ uptake prevents desynchronization of quantal release and minimizes depletion during repetitive stimulation of mouse motor nerve terminalsGavriel David
Department of Physiology and Biophysics, University of Miami School of Medicine, FL 33101, USA
J Physiol 548:425-38. 2003..Thus, mitochondrial Ca2+ uptake is essential for sustaining phasic release, and thus neuromuscular transmission, during and following tetanic stimulation...
Research Grants
- Ca2+ mishandling and ischemia-vulnerability in fALS model motor terminalsGavriel David; Fiscal Year: 2010..Treatments to preserve remaining motor nerve terminals should slow the progression of paralysis, and thus may become an important new component of therapies for treating ALS. ..