Current Search: Energy Metabolism (x)
View All Items
- Title
- Neuronal Energetics: Mitochondrial Distribution and The Phosphagen System.
- Creator
- Riboul, Danielle V., Macleod, Gregory T., Florida Atlantic University, Department of Biological Sciences, Charles E. Schmidt College of Science
- Abstract/Description
-
The relationship between neuronal function and energy metabolism is a field of intense inquiry and while bioenergetic per se are well understood, we lack a good understanding of the ways in which these mechanisms overcome the challenges presented by the unique morphology of neurons and their volatile energy demands. Here we examined the extent to which these challenges can be met through strategic mitochondrial placement and the support of a phosphagen system. We examined fluctuations in...
Show moreThe relationship between neuronal function and energy metabolism is a field of intense inquiry and while bioenergetic per se are well understood, we lack a good understanding of the ways in which these mechanisms overcome the challenges presented by the unique morphology of neurons and their volatile energy demands. Here we examined the extent to which these challenges can be met through strategic mitochondrial placement and the support of a phosphagen system. We examined fluctuations in energy demand of Drosophila larval motor neurons utilizing a combination of computational modeling and empirical analysis, and uncovered a neglected aspect of cellular energy metabolism that appears to accommodate the stress of highly volatile energy demands. Our findings highlight a reliance on the phosphagen system to buffer against rapid changes in the rate of ATP consumption induced by burst firing. The knockdown of a key element in the phosphagen system of invertebrates, arginine kinase, revealed a suppression of the mitochondrial proton motive force, and a more rapid decline in the presynaptic ATP/ADP ratio during burst firing. The knock down of arginine kinase also revealed metabolic shifts that indicated a compensatory increase in glycolysis, but, surprisingly, few consequences for either presynaptic Ca2+ handling or neurotransmission. In a final effort to ensure that we were imposing a metabolic load adequate to challenge these motor neurons, we developed an ex vivo calcium clearance assay and in vivo locomotor performance assay – currently in their final stages of validation.
Show less - Date Issued
- 2024
- PURL
- http://purl.flvc.org/fau/fd/FA00014419
- Subject Headings
- Mitochondria, Neurons, Energy metabolism
- Format
- Document (PDF)
- Title
- Energy metabolism and slow skeletal troponin I phosphorylation in cardiac troponin I null mouse heart.
- Creator
- Jia, Yuanyuan, Florida Atlantic University, Huang, Xupei, Charles E. Schmidt College of Medicine, Department of Biomedical Science
- Abstract/Description
-
Troponin I (TnI) plays an important role in cardiac muscle contraction. Two TnI genes (cardiac and slow skeletal TnI) are predominantly expressed in the heart. In cTnI knockout mice, myocardial TnI deficiency results in a diastolic dysfunction and a sudden death in homozygous mutants. In the present studies, energy metabolism has been analyzed in myocardial cells from cTnI null hearts. Our results have demonstrated that damaged relaxation and increased Ca2+-independent force production in...
Show moreTroponin I (TnI) plays an important role in cardiac muscle contraction. Two TnI genes (cardiac and slow skeletal TnI) are predominantly expressed in the heart. In cTnI knockout mice, myocardial TnI deficiency results in a diastolic dysfunction and a sudden death in homozygous mutants. In the present studies, energy metabolism has been analyzed in myocardial cells from cTnI null hearts. Our results have demonstrated that damaged relaxation and increased Ca2+-independent force production in cTnI null hearts stimulated myofibril MgATPase activities accompanied by the increase of mitochondria quantity and ATPase activities. In addition, an increase of ssTnI phosphorylation level has been observed in cTnI null hearts. The results indicate that TnI deficiency can cause the disturbance of energy metabolism and some protein overphosphorylation.
Show less - Date Issued
- 2003
- PURL
- http://purl.flvc.org/fcla/dt/12998
- Subject Headings
- Mice as laboratory animals, Mice--Metabolism, Energy metabolism, Mitochondria
- Format
- Document (PDF)
- Title
- The effect of ingesting a caffeine-enhanced sport drink on resting energy expenditures and blood pressure in females.
- Creator
- Klepacki, Brian, Graves, B. Sue, Hellberg, Peter
- Date Issued
- 2009-07-31
- PURL
- http://purl.flvc.org/fcla/dt/3327168
- Subject Headings
- Caffeine --Administration & Dosage, Energy Metabolism, Rest --Physiology, Blood Pressure, Blood Pressure --Physiology, Female, Dietary Supplements
- Format
- Document (PDF)