Article

Microdialysis of interstitial amino acids during spreading depression and anoxic depolarization in rat neocortex.

Department of Medical Physiology, University of Copenhagen, Denmark.
Brain Research (impact factor: 2.73). 06/1993; 612(1-2):61-9. DOI:10.1016/0006-8993(93)91644-8 pp.61-9
Source: PubMed

ABSTRACT We have examined the effect of cortical spreading depression (SD) and anoxic depolarization (AD) on the interstitial concentration changes of amino acids (AA) in the neocortex of anesthetized rats using microdialysis and HPLC. Accompanying SD alanine increased to 126 +/- 11%, arginine to 116 +/- 3%, aspartate to 160 +/- 17%, glutamate to 163 +/- 9%, glycine to 158 +/- 21%, serine to 125 +/- 9%, and taurine to 172 +/- 15% (mean +/- 1 S.E.M.). The increases lasted for about 1 min. Histidine decreased to 74% +/- 4% at 1 min following SD, and returned to normal 4 min later. Cardiac arrest triggered AD after approximately 2 min, immediately followed by changes of interstitial AAs. At 5 min after AD alanine had increased to 183 +/- 13%, aspartate to 3,458 +/- 656%, GABA to 338 +/- 35%, glutamate to 1,696 +/- 546%, glycine to 297 +/- 37%, serine to 153 +/- 12%, and taurine to 1721 +/- 98% as compared to control values (mean +/- 1 S.E.M.). Histidine decreased to 78 +/- 2% at 3 min following AD while arginine exhibited insignificant variations around the baseline. The increase of glutamate during SD is consistent with activation of NMDA-receptors as an essential requirement for this reaction. The increase of AAs may also contribute to the sequence of events leading to AD, though the exact mechanism remains unknown. SD is an important pathophysiological mechanism of the ischemic penumbra associated with focal cerebral ischemia, while AD reflects the electrophysiological status of the infarct core.(ABSTRACT TRUNCATED AT 250 WORDS)

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    Article: Kynurenine metabolites and migraine: experimental studies and therapeutic perspectives.
    Annamária Fejes, Arpád Párdutz, József Toldi, László Vécsei
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    ABSTRACT: Migraine is one of the commonest neurological disorders. Despite intensive research, its exact pathomechanism is still not fully understood and effective therapy is not always available. One of the key molecules involved in migraine is glutamate, whose receptors are found on the first-, second- and third-order trigeminal neurones and are also present in the migraine generators, including the dorsal raphe nucleus, nucleus raphe magnus, locus coeruleus and periaqueductal grey matter. Glutamate receptors are important in cortical spreading depression, which may be the electrophysiological correlate of migraine aura. The kynurenine metabolites, endogenous tryptophan metabolites, include kynurenic acid (KYNA), which exerts a blocking effect on ionotropic glutamate and α7-nicotinic acetylcholine receptors. Thus, KYNA and its derivatives may act as modulators at various levels of the pathomechanism of migraine. They can give rise to antinociceptive effects at the periphery, in the trigeminal nucleus caudalis, and may also act on migraine generators and cortical spreading depression. The experimental data suggest that KYNA or its derivatives might offer a novel approach to migraine therapy.
    DNA research: an international journal for rapid publication of reports on genes and genomes 06/2011; 9(2):376-87. · 1.73 Impact Factor
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Keywords

1 min
 
2 min
 
3 min
 
5 min
 
AAs
 
Accompanying SD alanine
 
AD alanine
 
amino acids
 
anesthetized rats
 
anoxic depolarization
 
arginine exhibited insignificant variations
 
Cardiac arrest
 
control values
 
essential requirement
 
focal cerebral ischemia
 
increases
 
infarct core.(ABSTRACT TRUNCATED
 
interstitial AAs
 
normal 4 min
 
pathophysiological mechanism
 

M Fabricius