Document Detail


Interaction between tissue oxygen tension and NADH imaging during synaptic stimulation and hypoxia in rat hippocampal slices.
MedLine Citation:
PMID:  15837126     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Oxygen and NADH are essential components in the production of ATP in the CNS. This study examined the dynamic interaction between tissue oxygen tension (pO(2)) and NADH imaging changes within hippocampal tissue slices, during metabolic stresses including hypoxia and synaptic activation. The initiation of abrupt hypoxia (from 95% O(2) to 95% N(2)) caused a rapid decrease in pO(2), onset of hypoxic spreading depression (hsd; at 6.7+/-1.3 mm Hg; n=15), and a monophasic increase in NADH. Provided that reoxygenation was prompt, synaptic responses, pO(2) and NADH levels returned to baseline following hsd. Longer hypoxia caused irreversible neuronal dysfunction, an increase in pO(2) beyond baseline (due to decreased tissue demand), and hyperoxidation of NADH (10+/-2% decrease below baseline; n=7). Synaptic activation in ambient 95% O(2) caused a decrease or 'initial dip' in pO(2) and a biphasic NADH response (oxidation followed by reduction). The oxidizing phase of the NADH response was mitochondrial as it was synchronous with the 'initial' dip in pO(2). Following slow graded reductions in ambient oxygen levels to 8%, four of seven slices developed hsd following synaptic stimulation. The hypoxic threshold for graded oxygen reductions occurred at 7.9+/-5.8 mm Hg O(2) (n=7). Our hypoxic threshold range (6.7-7.9 mm Hg O(2) from abrupt and graded oxygen reduction, respectively) correlates well with reported in vivo values of <12 mm Hg O(2). The major findings of this study include: 1) determination of the critical physiological threshold of pO(2) (based upon hsd), which is a marker of imminent neuronal death if oxygen is not rapidly restored; 2) NADH hyperoxidation and an increase in pO(2) beyond baseline levels following longer periods of hypoxia; and 3) the occurrence of a pO(2) 'dip' during synaptic stimulation, which correlates with the early oxidizing phase of the biphasic NADH response.
Authors:
K A Foster; C J Beaver; D A Turner
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Publication Detail:
Type:  Comparative Study; In Vitro; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Neuroscience     Volume:  132     ISSN:  0306-4522     ISO Abbreviation:  Neuroscience     Publication Date:  2005  
Date Detail:
Created Date:  2005-04-19     Completed Date:  2005-08-30     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  7605074     Medline TA:  Neuroscience     Country:  United States    
Other Details:
Languages:  eng     Pagination:  645-57     Citation Subset:  IM    
Affiliation:
Research and Surgery Services, Durham Veterans Affairs Medical Center, Durham, NC 27710, USA. fosterka@duke.edu
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MeSH Terms
Descriptor/Qualifier:
Analysis of Variance
Animals
Anoxia / physiopathology*
Brain Mapping
Diagnostic Imaging / methods
Electric Stimulation / methods
Electrodes
Hippocampus / metabolism*,  physiopathology,  radiation effects
Male
NAD / metabolism*
Oxygen / metabolism*
Rats
Rats, Inbred F344
Synaptic Transmission / physiology*,  radiation effects
Time Factors
Grant Support
ID/Acronym/Agency:
NS45304/NS/NINDS NIH HHS
Chemical
Reg. No./Substance:
53-84-9/NAD; 7782-44-7/Oxygen

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


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