| Mitochondria and neuronal activity. | |
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MedLine Citation:
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PMID: 17092996 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Mitochondria are central for various cellular processes that include ATP production, intracellular Ca(2+) signaling, and generation of reactive oxygen species. Neurons critically depend on mitochondrial function to establish membrane excitability and to execute the complex processes of neurotransmission and plasticity. While much information about mitochondrial properties is available from studies on isolated mitochondria and dissociated cell cultures, less is known about mitochondrial function in intact neurons in brain tissue. However, a detailed description of the interactions between mitochondrial function, energy metabolism, and neuronal activity is crucial for the understanding of the complex physiological behavior of neurons, as well as the pathophysiology of various neurological diseases. The combination of new fluorescence imaging techniques, electrophysiology, and brain slice preparations provides a powerful tool to study mitochondrial function during neuronal activity, with high spatiotemporal resolution. This review summarizes recent findings on mitochondrial Ca(2+) transport, mitochondrial membrane potential (DeltaPsi(m)), and energy metabolism during neuronal activity. We will first discuss interactions of these parameters for experimental stimulation conditions that can be related to the physiological range. We will then describe how mitochondrial and metabolic dysfunction develops during pathological neuronal activity, focusing on temporal lobe epilepsy and its experimental models. The aim is to illustrate that 1) the structure of the mitochondrial compartment is highly dynamic in neurons, 2) there is a fine-tuned coupling between neuronal activity and mitochondrial function, and 3) mitochondria are of central importance for the complex behavior of neurons. |
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Authors:
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Oliver Kann; Richard Kovács |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Review Date: 2006-11-08 |
Journal Detail:
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Title: American journal of physiology. Cell physiology Volume: 292 ISSN: 0363-6143 ISO Abbreviation: Am. J. Physiol., Cell Physiol. Publication Date: 2007 Feb |
Date Detail:
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Created Date: 2007-02-13 Completed Date: 2007-04-05 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 100901225 Medline TA: Am J Physiol Cell Physiol Country: United States |
Other Details:
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Languages: eng Pagination: C641-57 Citation Subset: IM |
Affiliation:
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Institut für Neurophysiologie, Charité-Universitätsmedizin Berlin, Tucholskystrasse 2, 10117 Berlin, Germany. oliver.kann@charite.de |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Brain / physiology* Calcium Signaling Epilepsy, Temporal Lobe / metabolism, physiopathology Humans Membrane Potential, Mitochondrial Mitochondria / physiology* Mitochondrial Diseases / metabolism, physiopathology Mitochondrial Proteins / metabolism Neurons / physiology* Oxygen Consumption / physiology Reactive Oxygen Species / metabolism Submitochondrial Particles / metabolism |
| Chemical | |
Reg. No./Substance:
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0/Mitochondrial Proteins; 0/Reactive Oxygen Species |
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