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Titolo:
Glycolysis prevents anoxia-induced synaptic transmission damage in rat hippocampal slices
Autore:
Tian, GF; Baker, AJ;
Indirizzi:
Univ Toronto, St Michaels Hosp, Cara Phelan Ctr Trauma Res, Traumat Brain Injury Lab, Toronto, ON M5B 1W8, Canada Univ Toronto Toronto ON Canada M5B1W8 y Lab, Toronto, ON M5B 1W8, Canada Univ Toronto, St Michaels Hosp, Dept Anaesthesia, Toronto, ON M5B 1W8, Canada Univ Toronto Toronto ON Canada M5B 1W8 hesia, Toronto, ON M5B 1W8, Canada
Titolo Testata:
JOURNAL OF NEUROPHYSIOLOGY
fascicolo: 4, volume: 83, anno: 2000,
pagine: 1830 - 1839
SICI:
0022-3077(200004)83:4<1830:GPASTD>2.0.ZU;2-8
Fonte:
ISI
Lingua:
ENG
Soggetto:
EXTRACELLULAR POTASSIUM; FUNCTIONAL RECOVERY; NEURAL ACTIVITY; BRAIN LACTATE; IN-VITRO; HYPOXIA; NEURONS; GLUCOSE; INVITRO; DEPRIVATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
47
Recensione:
Indirizzi per estratti:
Indirizzo: Tian, GF Univ Toronto, St Michaels Hosp, Cara Phelan Ctr Trauma Res, Traumat Brain Injury Lab, Rm 7080,7th Fl,Bond Wing,30 Bond St, Toronto, ON M5B 1W8, Canada Univ Toronto Rm 7080,7th Fl,Bond Wing,30 Bond St Toronto ON Canada M5B 1W8
Citazione:
G.F. Tian e A.J. Baker, "Glycolysis prevents anoxia-induced synaptic transmission damage in rat hippocampal slices", J NEUROPHYS, 83(4), 2000, pp. 1830-1839

Abstract

Prolonged anoxia can cause permanent damage to synaptic transmission in the mammalian CNS. We tested the hypothesis that lack of glucose is the majorcause of irreversible anoxic transmission damage, and that anoxic synaptictransmission damage could be prevented by glycolysis in rat hippocampal slices. The evoked population spike (PS) was extracellularly recorded in the CAI pyramidal cell layer after stimulation of the Schaffer collaterals. When the slice was superfused with artificial cerebrospinal fluid (ACSF) containing 4 mM glucose, following 10 min anoxia, the evoked PS did not recover at all after 60 min reoxygenation. When superfusion ACSF contained 10 mM glucose with or without 0.5 mM alpha-cyano-4-hydroxycinnate (4-CIN), after 60min reoxygenation the evoked PS completely recovered following 10 min anoxia. When superfusion ACSF contained 20 mM glucose with or without 1 mM sodium cyanide (NaCN), after 60 min reoxygenation the evoked PS completely recovered even following 120 min anoxia. In contrast, when superfusion ACSF contained 4 mM glucose, following 10 min 1 mM NaCN chemical anoxia alone, without anoxic anoxia, the evoked PS displayed no recovery after 60 min reoxygenation. Moreover, when 16 mM mannitol and 16 sodium L-lactate were added into 4 mM glucose ACSF, following 10 min anoxia the evoked PS failed to recover at all after 60 min reoxygenation. The results indicate that elevated glucose concentration powerfully protected the synaptic transmission against anoxic damage, and the powerful protection is due to anaerobic metabolism of glucose and not a result of the higher osmolality in higher glucose ACSF. We conclude that lack of glucose is the major cause of anoxia-induced synaptic transmission damage, and that if sufficient glucose is supplied, glycolysis could prevent this damage in vitro.

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Documento generato il 27/01/20 alle ore 01:29:45