Implications of glial nitric oxyde in neurodegenerative diseases
Nitric oxide (NO) is a pleiotropic janus-faced molecule synthesized by nitric oxide synthases (NOS) which plays a critical role in a number of physiological and pathological processes in humans. The physiological roles of NO depend on its local concentrations, as well as its availability and the nat...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2015-08-01
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| Series: | Frontiers in Cellular Neuroscience |
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| Online Access: | http://journal.frontiersin.org/Journal/10.3389/fncel.2015.00322/full |
| _version_ | 1818474863270035456 |
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| author | Jose Enrique eYuste Ernesto eTarragon Carmen María eCampuzano Francisco eRos Bernal |
| author_facet | Jose Enrique eYuste Ernesto eTarragon Carmen María eCampuzano Francisco eRos Bernal |
| author_sort | Jose Enrique eYuste |
| collection | DOAJ |
| description | Nitric oxide (NO) is a pleiotropic janus-faced molecule synthesized by nitric oxide synthases (NOS) which plays a critical role in a number of physiological and pathological processes in humans. The physiological roles of NO depend on its local concentrations, as well as its availability and the nature of downstream target molecules. Its double-edged sword action has been linked to neurodegenerative disorders. Excessive NO production, as the evoked by inflammatory signals, has been identified as one of the major causative reasons for the pathogenesis of several neurodegenerative diseases. Moreover, excessive NO synthesis under neuroinflammation leads to the formation of reactive nitrogen species and neuronal cell death. There is an intimate relation between microglial activation, NO and neuroinflammation in the human brain. The role of NO in neuroinflammation has been defined in animal models where this neurotransmitter can modulate the inflammatory process acting on key regulatory pathways, such as those associated with excitotoxicity processes induced by glutamate accumulation and microglial activation. Activated glia express inducible NOS and produce NO that triggers calcium mobilization from the endoplasmic reticulum, activating the release of vesicular glutamate from astroglial cells resulting in neuronal death. This change in microglia potentially contributes to the increased age-associated susceptibility and neurodegeneration. In the current review, information is provided about the role of NO, glial activation and age-related processes in the central nervous system (CNS) that may be helpful in the isolation of new therapeutic targets for aging and neurodegenerative diseases. |
| first_indexed | 2024-04-14T04:42:55Z |
| format | Article |
| id | doaj.art-a831ee4ebc7048e6b64fed90b2bf484d |
| institution | Directory Open Access Journal |
| issn | 1662-5102 |
| language | English |
| last_indexed | 2024-04-14T04:42:55Z |
| publishDate | 2015-08-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Cellular Neuroscience |
| spelling | doaj.art-a831ee4ebc7048e6b64fed90b2bf484d2022-12-22T02:11:36ZengFrontiers Media S.A.Frontiers in Cellular Neuroscience1662-51022015-08-01910.3389/fncel.2015.00322152023Implications of glial nitric oxyde in neurodegenerative diseasesJose Enrique eYuste0Ernesto eTarragon1Carmen María eCampuzano2Francisco eRos Bernal3University Jaume IUniversité de LiègeUniversity Jaume IUniversity Jaume INitric oxide (NO) is a pleiotropic janus-faced molecule synthesized by nitric oxide synthases (NOS) which plays a critical role in a number of physiological and pathological processes in humans. The physiological roles of NO depend on its local concentrations, as well as its availability and the nature of downstream target molecules. Its double-edged sword action has been linked to neurodegenerative disorders. Excessive NO production, as the evoked by inflammatory signals, has been identified as one of the major causative reasons for the pathogenesis of several neurodegenerative diseases. Moreover, excessive NO synthesis under neuroinflammation leads to the formation of reactive nitrogen species and neuronal cell death. There is an intimate relation between microglial activation, NO and neuroinflammation in the human brain. The role of NO in neuroinflammation has been defined in animal models where this neurotransmitter can modulate the inflammatory process acting on key regulatory pathways, such as those associated with excitotoxicity processes induced by glutamate accumulation and microglial activation. Activated glia express inducible NOS and produce NO that triggers calcium mobilization from the endoplasmic reticulum, activating the release of vesicular glutamate from astroglial cells resulting in neuronal death. This change in microglia potentially contributes to the increased age-associated susceptibility and neurodegeneration. In the current review, information is provided about the role of NO, glial activation and age-related processes in the central nervous system (CNS) that may be helpful in the isolation of new therapeutic targets for aging and neurodegenerative diseases.http://journal.frontiersin.org/Journal/10.3389/fncel.2015.00322/fullNitric OxideNeuroinflammationNeurodegenerative disordersNeuronal DeathNeuronal nitric oxide |
| spellingShingle | Jose Enrique eYuste Ernesto eTarragon Carmen María eCampuzano Francisco eRos Bernal Implications of glial nitric oxyde in neurodegenerative diseases Frontiers in Cellular Neuroscience Nitric Oxide Neuroinflammation Neurodegenerative disorders Neuronal Death Neuronal nitric oxide |
| title | Implications of glial nitric oxyde in neurodegenerative diseases |
| title_full | Implications of glial nitric oxyde in neurodegenerative diseases |
| title_fullStr | Implications of glial nitric oxyde in neurodegenerative diseases |
| title_full_unstemmed | Implications of glial nitric oxyde in neurodegenerative diseases |
| title_short | Implications of glial nitric oxyde in neurodegenerative diseases |
| title_sort | implications of glial nitric oxyde in neurodegenerative diseases |
| topic | Nitric Oxide Neuroinflammation Neurodegenerative disorders Neuronal Death Neuronal nitric oxide |
| url | http://journal.frontiersin.org/Journal/10.3389/fncel.2015.00322/full |
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