Document Detail


Nitric oxide signaling in brain function, dysfunction, and dementia.
MedLine Citation:
PMID:  20817920     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Nitric oxide (NO) is an important signaling molecule that is widely used in the nervous system. With recognition of its roles in synaptic plasticity (long-term potentiation, LTP; long-term depression, LTD) and elucidation of calcium-dependent, NMDAR-mediated activation of neuronal nitric oxide synthase (nNOS), numerous molecular and pharmacological tools have been used to explore the physiology and pathological consequences for nitrergic signaling. In this review, the authors summarize the current understanding of this subtle signaling pathway, discuss the evidence for nitrergic modulation of ion channels and homeostatic modulation of intrinsic excitability, and speculate about the pathological consequences of spillover between different nitrergic compartments in contributing to aberrant signaling in neurodegenerative disorders. Accumulating evidence points to various ion channels and particularly voltage-gated potassium channels as signaling targets, whereby NO mediates activity-dependent control of intrinsic neuronal excitability; such changes could underlie broader mechanisms of synaptic plasticity across neuronal networks. In addition, the inability to constrain NO diffusion suggests that spillover from endothelium (eNOS) and/or immune compartments (iNOS) into the nervous system provides potential pathological sources of NO and where control failure in these other systems could have broader neurological implications. Abnormal NO signaling could therefore contribute to a variety of neurodegenerative pathologies such as stroke/excitotoxicity, Alzheimer's disease, multiple sclerosis, and Parkinson's disease.
Authors:
Joern R Steinert; Tatyana Chernova; Ian D Forsythe
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry     Volume:  16     ISSN:  1089-4098     ISO Abbreviation:  Neuroscientist     Publication Date:  2010 Aug 
Date Detail:
Created Date:  2010-09-06     Completed Date:  2011-01-07     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9504819     Medline TA:  Neuroscientist     Country:  United States    
Other Details:
Languages:  eng     Pagination:  435-52     Citation Subset:  IM    
Affiliation:
Neurotoxicity at the Synaptic Interface, MRC Toxicology Unit, University of Leicester, Leicester, UK.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Brain / metabolism*
Dementia / metabolism*
Neuronal Plasticity / physiology
Neurons / metabolism
Nitric Oxide / metabolism*
Signal Transduction / physiology
Synaptic Transmission / physiology*
Grant Support
ID/Acronym/Agency:
//Medical Research Council
Chemical
Reg. No./Substance:
10102-43-9/Nitric Oxide

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Go or stop? Divergent roles of Reelin in radial neuronal migration.
Next Document:  CRASH syndrome: does it teach us about neurotrophic functions of cell adhesion molecules?