Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Changes in the calcium dependence of glutamate transmission in the hippocampal CA1 region after brief hypoxia-hypoglycemia
Autore:
Ouanonou, A; Zhang, Y; Zhang, L;
Indirizzi:
Univ Toronto, Playfair Neurosci Unit, Western Div,Dept Med Neurol, TorontoHosp,Bloorview Epilepsy Program,Res Inst, Toronto, ON M5T 2S8, Canada Univ Toronto Toronto ON Canada M5T 2S8 Inst, Toronto, ON M5T 2S8, Canada
Titolo Testata:
JOURNAL OF NEUROPHYSIOLOGY
fascicolo: 3, volume: 82, anno: 1999,
pagine: 1147 - 1155
SICI:
0022-3077(199909)82:3<1147:CITCDO>2.0.ZU;2-1
Fonte:
ISI
Lingua:
ENG
Soggetto:
LONG-TERM POTENTIATION; PERMEANT CA2+ CHELATORS; EXCITATORY POSTSYNAPTIC CURRENTS; TRANSIENT FOREBRAIN ISCHEMIA; PAIRED-PULSE FACILITATION; IN-VITRO ISCHEMIA; RAT-BRAIN SLICES; SYNAPTIC TRANSMISSION; NMDA RECEPTOR; TRANSMITTER RELEASE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
72
Recensione:
Indirizzi per estratti:
Indirizzo: Zhang, L Univ Toronto, Playfair Neurosci Unit, Western Div,Dept Med Neurol, TorontoHosp,Bloorview Epilepsy Program,Res Inst, Room McL 13-411,399 Bathurst St,Toronto, ON M5T 2S8, Canada Univ Toronto Room McL 13-411,399 Bathurst St Toronto ON Canada M5T 2S8
Citazione:
A. Ouanonou et al., "Changes in the calcium dependence of glutamate transmission in the hippocampal CA1 region after brief hypoxia-hypoglycemia", J NEUROPHYS, 82(3), 1999, pp. 1147-1155

Abstract

Using the model of hypoxia-hypoglycemia (HH) in rat brain slices, we askedwhether glutamate transmission is altered following a brief HH episode. The HH challenge was conducted by exposing slices to a glucose-free medium aerated with 95% N-2-5% CO2, for similar to 4 min, and glutamate transmissionin the hippocampal CA1 region was monitored at different post HH times. Inslices examined less than or equal to 8 h post I-III, CA1 synaptic field potentials are comparable in amplitude to controls, but are less sensitive to experimental manipulations designed to attenuate intracellular Ca2+ signals, as compared with controls. Reducing calcium influx, by applying a nonspecific calcium channel blocker Co2+ Or lowering external Ca2+, attenuated CA1 synaptic potentials much less in challenged slices than in controls. Buffering intracellular Ca2+ by bis-(o-aminophenoxy)-N,N,N',N'-tetraacetic acid-AM (BAPTA-AM) attenuated CA1 synaptic potentials in control but not in slices post HH. Furthermore, minimally evoked excitatory postsynaptic currents displayed a lower failure rate in post-hypoxic CA1 neurons compared with controls. Based on these convergent observations, we suggest that evoked CA1 glutamate transmission is altered in the first several hours after brief hypoxia, likely resulting from alterations in intracellular Ca2+ homeostasis and/or Ca2+-dependent processes governing transmitter release.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 15/07/20 alle ore 13:29:02