Financiado en parte por Daiichi Sankyo Foundation of Life Science, Daiichi Sankyo Europe
Synergistic action of dendritic mitochondria and creatine kinase maintains ATP homeostasis and actin dynamics in growing neuronal dendrites
Fukumitsu K, Fujishima K, Yoshimura A, Wu YK, Heuser J, Kengaku M
The Journal of neuroscience : the official journal of the Society for Neuroscience · 75 citas
Etiquetas de revisión
Financiado por la industriaSolo mecanismosDatos neutrales que nuestra revisión registró sobre cómo se hizo este estudio. Describen el método, nunca si nos gusta el resultado.
Cómo se estudió
- Diseño
- Estudio en animales (clasificado por nuestro filtro de IA)
- Estudiado en
- Animales
- Resultado principal
- Solo mecanismos
Quién lo pagó
- Financiación
- Financiado por la industria
- Empresa
- Daiichi Sankyo Foundation of Life Science
- Gobierno
- Japan Society for the Promotion of Science
- Empresa
- Daiichi Sankyo Europe
- Subvenciones
- Japan Society for the Promotion of Science (25830011); Japan Society for the Promotion of Science (26290005)
Según 3 financiadores declarados.
Publicación
- Publicado
- 2015-04-08 · J Neurosci · vol. 35 · número 14 · págs. 5707–5723
- Editorial
- Society for Neuroscience
- Citado
- 83 citas · más que el 95% de estudios similares · 4.0× el promedio de su campo
- Impacto
- Entre el 10 % más citado de su campo
- Referencias
- 78 trabajos
- Acceso
- Acceso abierto (revista híbrida) · CC-BY-NC-SA
- Áreas de investigación
- Neuroscience and Neuropharmacology Research · Mitochondrial Function and Pathology · Retinal Development and Disorders
- Palabras clave
- Mitochondrion, Cell biology, Cofilin, Phosphocreatine, Cytosol, Biology, Dendritic spine, Dendrite (mathematics), Actin remodeling of neurons, Cytoskeleton, Chemistry, Actin cytoskeleton, Neuroscience, Biochemistry, Cell
- MeSH
- cerebellum, hippocampus, neurons, dendrites, cells, cultured, mitochondria, animals, mice, inbred icr, humans, mice, dependovirus, egtazic acid, actins, creatine kinase, deoxyglucose, carrier proteins, luminescent proteins, nerve tissue proteins, adenosine triphosphate, calcium channel blockers, chelating agents, pregnancy, female, male, membrane potential, mitochondrial
6 autores
- Kansai Fukumitsu🇯🇵🇺🇸Kyoto University; Material Sciences (United States)
- Kazuto Fujishima🇺🇸Material Sciences (United States)
- Azumi Yoshimura🇺🇸Material Sciences (United States)
- You Kure Wu🇯🇵🇺🇸Kyoto University; Material Sciences (United States)
- John Heuser🇺🇸Material Sciences (United States)
- Mineko Kengaku🇯🇵🇺🇸Kyoto University; Material Sciences (United States)
Resumen
El texto original del estudio, en el idioma en que se publicó.
The distribution of mitochondria within mature, differentiated neurons is clearly adapted to their regional physiological needs and can be perturbed under various pathological conditions, but the function of mitochondria in developing neurons has been less well studied. We have studied mitochondrial distribution within developing mouse cerebellar Purkinje cells and have found that active delivery of mitochondria into their dendrites is a prerequisite for proper dendritic outgrowth. Even when mitochondria in the Purkinje cell bodies are functioning normally, interrupting the transport of mitochondria into their dendrites severely disturbs dendritic growth. Additionally, we find that the growth of atrophic dendrites lacking mitochondria can be rescued by activating ATP-phosphocreatine exchange mediated by creatine kinase (CK). Conversely, inhibiting cytosolic CKs decreases dendritic ATP levels and also disrupts dendrite development. Mechanistically, this energy depletion appears to perturb normal actin dynamics and enhance the aggregation of cofilin within growing dendrites, reminiscent of what occurs in neurons overexpressing the dephosphorylated form of cofilin. These results suggest that local ATP synthesis by dendritic mitochondria and ATP-phosphocreatine exchange act synergistically to sustain the cytoskeletal dynamics necessary for dendritic development.
Resumen vía Europe PMC. Los derechos de autor siguen siendo de los autores o la editorial (CC BY-NC-SA).
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