Difference between revisions of "Flatters 2015 Prog Mol Biol Transl Sci"
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{{Publication | {{Publication | ||
|title=Flatters SJ (2015) The contribution of mitochondria to sensory processing and pain. Prog Mol Biol Transl Sci 131:119-46. | |title=Flatters SJ (2015) The contribution of mitochondria to sensory processing and pain. Prog Mol Biol Transl Sci 131:119-46. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/25744672 PMID:25744672] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/25744672 PMID:25744672] | ||
|authors=Flatters SJ | |authors=Flatters SJ | ||
|year=2015 | |year=2015 | ||
|journal=Prog Mol Biol Transl Sci | |journal=Prog Mol Biol Transl Sci | ||
|abstract=Mitochondria have a variety of essential functions within neurons including oxygen consumption, ATP generation, calcium buffering, and reactive oxygen species (ROS) generation. Despite extensive research into the contribution of mitochondrial function in other neurological disorders such as Parkinson's disease, the role of mitochondrial function in sensory processing and pain has been relatively unexplored until recent years. As this area of pain research is in its infancy, this review will be a descriptive summary-rather than a critical review-of data that suggests mitochondrial function/dysfunction as a causal or contributory mechanism of normal sensory processing and chronic pain. Evidence for mitochondrial dysfunction from both chronic pain patients and animal models of chronic pain will be described. Such evidence involves different aspects of mitochondria and their function including mitochondrial ultrastructure, distribution, oxygen consumption, oxidative phosphorylation, calcium buffering, ROS, and ATP levels. Most recently, substantial amounts of data have demonstrated mitochondrial involvement in painful peripheral neuropathies evoked by chemotherapy, diabetes, and HIV and these topics will be particularly highlighted in this review. | |abstract=Mitochondria have a variety of essential functions within neurons including oxygen consumption, ATP generation, calcium buffering, and reactive oxygen species (ROS) generation. Despite extensive research into the contribution of mitochondrial function in other neurological disorders such as Parkinson's disease, the role of mitochondrial function in sensory processing and pain has been relatively unexplored until recent years. As this area of pain research is in its infancy, this review will be a descriptive summary-rather than a critical review-of data that suggests mitochondrial function/dysfunction as a causal or contributory mechanism of normal sensory processing and chronic pain. Evidence for mitochondrial dysfunction from both chronic pain patients and animal models of chronic pain will be described. Such evidence involves different aspects of mitochondria and their function including mitochondrial ultrastructure, distribution, oxygen consumption, oxidative phosphorylation, calcium buffering, ROS, and ATP levels. Most recently, substantial amounts of data have demonstrated mitochondrial involvement in painful peripheral neuropathies evoked by chemotherapy, diabetes, and HIV and these topics will be particularly highlighted in this review. | ||
|keywords=Calcium buffering, Chemotherapy-induced neuropathy, DRG, Diabetic neuropathy, HIV-associated neuropathy, Mitochondria, Mitochondrial bioenergetics, Neuron, Pain, ROS | |keywords=Calcium buffering, Chemotherapy-induced neuropathy, DRG, Diabetic neuropathy, HIV-associated neuropathy, Mitochondria, Mitochondrial bioenergetics, Neuron, Pain, ROS | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
|area=mt-Medicine, | |area=Respiration, mt-Medicine | ||
|diseases=Diabetes, Other | |||
|organism=Rat | |organism=Rat | ||
|tissues=Nervous system | |tissues=Nervous system | ||
|preparations=Homogenate, Isolated mitochondria | |preparations=Homogenate, Isolated mitochondria | ||
|enzymes=Complex I, Complex IV;cytochrome c oxidase, Complex V;ATP synthase | |enzymes=Complex I, Complex IV;cytochrome c oxidase, Complex V;ATP synthase | ||
|couplingstates=OXPHOS, ET | |||
|couplingstates= | |pathways=N, S, CIV, NS | ||
| | |||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
}} | }} | ||
Latest revision as of 17:58, 9 November 2017
| Flatters SJ (2015) The contribution of mitochondria to sensory processing and pain. Prog Mol Biol Transl Sci 131:119-46. |
Flatters SJ (2015) Prog Mol Biol Transl Sci
Abstract: Mitochondria have a variety of essential functions within neurons including oxygen consumption, ATP generation, calcium buffering, and reactive oxygen species (ROS) generation. Despite extensive research into the contribution of mitochondrial function in other neurological disorders such as Parkinson's disease, the role of mitochondrial function in sensory processing and pain has been relatively unexplored until recent years. As this area of pain research is in its infancy, this review will be a descriptive summary-rather than a critical review-of data that suggests mitochondrial function/dysfunction as a causal or contributory mechanism of normal sensory processing and chronic pain. Evidence for mitochondrial dysfunction from both chronic pain patients and animal models of chronic pain will be described. Such evidence involves different aspects of mitochondria and their function including mitochondrial ultrastructure, distribution, oxygen consumption, oxidative phosphorylation, calcium buffering, ROS, and ATP levels. Most recently, substantial amounts of data have demonstrated mitochondrial involvement in painful peripheral neuropathies evoked by chemotherapy, diabetes, and HIV and these topics will be particularly highlighted in this review. • Keywords: Calcium buffering, Chemotherapy-induced neuropathy, DRG, Diabetic neuropathy, HIV-associated neuropathy, Mitochondria, Mitochondrial bioenergetics, Neuron, Pain, ROS
Labels: MiParea: Respiration, mt-Medicine
Pathology: Diabetes, Other
Organism: Rat Tissue;cell: Nervous system Preparation: Homogenate, Isolated mitochondria Enzyme: Complex I, Complex IV;cytochrome c oxidase, Complex V;ATP synthase
Coupling state: OXPHOS, ET Pathway: N, S, CIV, NS HRR: Oxygraph-2k
