Ca2+, mitochondria and selective motoneuron vulnerability : implications for ALS
Motoneurons are selectively damaged in amyotrophic lateral sclerosis (ALS), a fatal neurodegenerative disorder. Although the underlying mechanisms are not completely understood, increasing evidence indicates that motoneurons are particularly sensitive to disruption of mitochondria and Ca(2+)-depende...
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| Veröffentlicht in: | Trends in neurosciences (Regular ed.) 2005-09, Vol.28 (9), p.494-500 |
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| container_title | Trends in neurosciences (Regular ed.) |
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| creator | VON LEWINSKIL, Friederike KELLER, Bernhard U |
| description | Motoneurons are selectively damaged in amyotrophic lateral sclerosis (ALS), a fatal neurodegenerative disorder. Although the underlying mechanisms are not completely understood, increasing evidence indicates that motoneurons are particularly sensitive to disruption of mitochondria and Ca(2+)-dependent signalling cascades. Comparison of ALS-vulnerable and ALS-resistant neurons identified low Ca(2+)-buffering capacity and a strong impact of mitochondrial signal cascades as important risk factors. Under physiological conditions, weak Ca(2+) buffers are valuable because they facilitate rapid relaxation times of Ca(2+) transients in motoneurons during high-frequency rhythmic activity. However, under pathological conditions, weak Ca(2+) buffers are potentially dangerous because they accelerate a vicious circle of mitochondrial disruption, Ca(2+) disregulation and excitotoxic cell damage. |
| doi_str_mv | 10.1016/j.tins.2005.07.001 |
| format | Article |
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Although the underlying mechanisms are not completely understood, increasing evidence indicates that motoneurons are particularly sensitive to disruption of mitochondria and Ca(2+)-dependent signalling cascades. Comparison of ALS-vulnerable and ALS-resistant neurons identified low Ca(2+)-buffering capacity and a strong impact of mitochondrial signal cascades as important risk factors. Under physiological conditions, weak Ca(2+) buffers are valuable because they facilitate rapid relaxation times of Ca(2+) transients in motoneurons during high-frequency rhythmic activity. However, under pathological conditions, weak Ca(2+) buffers are potentially dangerous because they accelerate a vicious circle of mitochondrial disruption, Ca(2+) disregulation and excitotoxic cell damage.</description><identifier>ISSN: 0166-2236</identifier><identifier>EISSN: 1878-108X</identifier><identifier>DOI: 10.1016/j.tins.2005.07.001</identifier><identifier>PMID: 16026864</identifier><identifier>CODEN: TNSCDR</identifier><language>eng</language><publisher>Oxford: Elsevier Science</publisher><subject>Amyotrophic lateral sclerosis ; Amyotrophic Lateral Sclerosis - metabolism ; Amyotrophic Lateral Sclerosis - pathology ; Animals ; Biological and medical sciences ; Brain - metabolism ; Brain - pathology ; Calcium - metabolism ; Cell physiology ; Cells ; Diseases of striated muscles. Neuromuscular diseases ; Fundamental and applied biological sciences. 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Although the underlying mechanisms are not completely understood, increasing evidence indicates that motoneurons are particularly sensitive to disruption of mitochondria and Ca(2+)-dependent signalling cascades. Comparison of ALS-vulnerable and ALS-resistant neurons identified low Ca(2+)-buffering capacity and a strong impact of mitochondrial signal cascades as important risk factors. Under physiological conditions, weak Ca(2+) buffers are valuable because they facilitate rapid relaxation times of Ca(2+) transients in motoneurons during high-frequency rhythmic activity. However, under pathological conditions, weak Ca(2+) buffers are potentially dangerous because they accelerate a vicious circle of mitochondrial disruption, Ca(2+) disregulation and excitotoxic cell damage.</description><subject>Amyotrophic lateral sclerosis</subject><subject>Amyotrophic Lateral Sclerosis - metabolism</subject><subject>Amyotrophic Lateral Sclerosis - pathology</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Brain - metabolism</subject><subject>Brain - pathology</subject><subject>Calcium - metabolism</subject><subject>Cell physiology</subject><subject>Cells</subject><subject>Diseases of striated muscles. Neuromuscular diseases</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Mitochondria - metabolism</subject><subject>Mitochondria - pathology</subject><subject>Models, Neurological</subject><subject>Molecular and cellular biology</subject><subject>Motor Neurons - metabolism</subject><subject>Motor Neurons - pathology</subject><subject>Neurology</subject><subject>Neurons</subject><subject>Reactive Oxygen Species</subject><subject>Secretion. 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| subjects | Amyotrophic lateral sclerosis Amyotrophic Lateral Sclerosis - metabolism Amyotrophic Lateral Sclerosis - pathology Animals Biological and medical sciences Brain - metabolism Brain - pathology Calcium - metabolism Cell physiology Cells Diseases of striated muscles. Neuromuscular diseases Fundamental and applied biological sciences. Psychology Humans Medical sciences Mitochondria - metabolism Mitochondria - pathology Models, Neurological Molecular and cellular biology Motor Neurons - metabolism Motor Neurons - pathology Neurology Neurons Reactive Oxygen Species Secretion. Exocytosis Spinal Cord - metabolism Spinal Cord - pathology |
| title | Ca2+, mitochondria and selective motoneuron vulnerability : implications for ALS |
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