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Titolo:
Anoxic depolarization mediates acute damage independent of glutamate in neocortical brain slices
Autore:
Jarvis, CR; Anderson, TR; Andrew, RD;
Indirizzi:
Queens Univ, Dept Anat & Cell Biol, Kingston, ON K7L 3N6, Canada Queens Univ Kingston ON Canada K7L 3N6 Biol, Kingston, ON K7L 3N6, Canada
Titolo Testata:
CEREBRAL CORTEX
fascicolo: 3, volume: 11, anno: 2001,
pagine: 249 - 259
SICI:
1047-3211(200103)11:3<249:ADMADI>2.0.ZU;2-Y
Fonte:
ISI
Lingua:
ENG
Soggetto:
INTRINSIC OPTICAL SIGNALS; CORTICAL SPREADING DEPRESSION; HIGH EXTRACELLULAR GLUTAMATE; ACUTE EXCITOTOXIC INSULT; MIDDLE CEREBRAL-ARTERY; HIPPOCAMPAL SLICES; OXYGEN/GLUCOSE DEPRIVATION; POSTISCHEMIC HYPOTHERMIA; NEUROLOGICAL DISORDERS; NEURONAL DAMAGE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
63
Recensione:
Indirizzi per estratti:
Indirizzo: Andrew, RD Queens Univ, Dept Anat & Cell Biol, Kingston, ON K7L 3N6, Canada Queens Univ Kingston ON Canada K7L 3N6 ton, ON K7L 3N6, Canada
Citazione:
C.R. Jarvis et al., "Anoxic depolarization mediates acute damage independent of glutamate in neocortical brain slices", CEREB CORT, 11(3), 2001, pp. 249-259

Abstract

An important but poorly understood event associated with ischemia is anoxic depolarization (AD), a sudden and profound depolarization of neurons and glia in cortical and subcortical gray matter. Leao first measured the AD asa wave of electrical silence moving across the cerebral cortex in 1947 andnoted its similarity to spreading depression (SD), SD is harmless when coursing through normoxic cortical tissue as during migraine aura. However for3-4 h following focal ischemia, the additional metabolic stress arising from recurring SD in the penumbra expands the ischemic core, so SD blockade is potentially beneficial therapeutically. In the present study, we measuredintrinsic optical signals (IOSs) to monitor anoxic depolarization in submerged rat neocortical slices during O-2/glucose deprivation (OGD), After similar to6 min of OGD, the AD was imaged as a focal increase in light transmittance which then propagated across neocortical gray at similar to2 mm/min. Although the slice was globally stressed, the AD always initiated focally,sometimes at multiple sites. Its propagation was coincident with a transient negative shift in the extracellular potential, the electrical signature of AD. Acute damage to neocortex (measured as a delayed decrease in LT and as a loss of the evoked field potential) followed only where the AD had propagated, so it is the combined metabolic demands of AD and OGD that acutelydamages all layers of the neocortex, Glutamate receptor antagonists (2 mM kynurenate or 25 muM AP-5/10 muM CNQX) did not block AD initiation, slow its propagation or prevent post-AD damage. This study shows that acute ischemic damage is greatly exacerberated by AD during metabolic stress and that glutamate receptor antagonists are not protective. Using this slice model, therapeutically tolerable drugs that block the AD and SD can be investigated.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 22/01/20 alle ore 12:22:24