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Titolo:
VOLATILE ANESTHETICS DEPRESS GLUTAMATE TRANSMISSION VIA PRESYNAPTIC ACTIONS
Autore:
MACIVER MB; MIKULEC AA; AMAGASU SM; MONROE FA;
Indirizzi:
STANFORD UNIV,SCH MED,DEPT ANESTHESIA STANFORD CA 94305
Titolo Testata:
Anesthesiology
fascicolo: 4, volume: 85, anno: 1996,
pagine: 823 - 834
SICI:
0003-3022(1996)85:4<823:VADGTV>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
LONG-TERM POTENTIATION; EXCITATORY SYNAPTIC TRANSMISSION; PAIRED-PULSE FACILITATION; RAT HIPPOCAMPUS; CA1 REGION; NEURONAL INHIBITION; CHANNEL COMPLEX; DENTATE GYRUS; AMINO-ACID; RELEASE;
Keywords:
ANESTHETICS, VOLATILE, HALOTHANE, ISOFLURANE; BRAIN CA1 NEURON, HIPPOCAMPAL SLICES, SYNAPSES, SYNAPTIC TRANSMISSION MEASUREMENT TECHNIQUES, ELECTROPHYSIOLOGIC RECORDINGS, EPSP FACILITATION NEUROTRANSMITTERS, GLUTAMATE, RELEASE, GABA;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
54
Recensione:
Indirizzi per estratti:
Citazione:
M.B. Maciver et al., "VOLATILE ANESTHETICS DEPRESS GLUTAMATE TRANSMISSION VIA PRESYNAPTIC ACTIONS", Anesthesiology, 85(4), 1996, pp. 823-834

Abstract

Background: Recent evidence for a presynaptic depression of glutamaterelease produced by volatile anesthetics prompted the current study of isoflurane and halothane effects on glutamate-mediated transmission in the mammalian central nervous system. Methods: Electrophysiologic recordings from CAI neurons In rat hippocampal brain slices were used to measure anesthetic effects on glutamate-mediated excitatory postsynaptic potential (EPSP) amplitudes and paired pulse facilitation. Pairedpulse facilitation is known to be altered when the calcium-dependent release of glutamate is depressed, but not when EPSP amplitudes are depressed by postsynaptic mechanisms. Results: Isoflurane depressed EPSPamplitudes over a concentration range of 0.35-2.8 vol %, with a 50% depression (EC(50)) occurring at 1.0 vol % (0.71 rat minimum alveolar concentration). This depression was accompanied by an increase in paired-pulse facilitation of similar to 30% at 1.7 vol %, using interpulse intervals of 120 ms. Halothane depressed EPSP amplitudes in a concentration-dependent manner (0.3-2.4 vol %, EC(50) = 1.1 minimum alveolar concentration; 1.3 vol %) and also increased facilitation by similar to20% at 1.2 vol %. These effects persisted in the presence of 10 mu M bicuculline, indicating that enhanced gamma-aminobutyric acid-mediatedinhibition was not involved. The anesthetic-induced increase in facilitation and EPSP depression was mimicked by lowering extracellular calcium, which is known to depress glutamate release at these synapses. The postsynaptic glutamate receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione depressed EPSP amplitudes with no change in facilitation.Conclusions: Our results confirm earlier findings that clinically relevant concentrations of volatile anesthetics depress glutamate-mediatedsynaptic transmission. The observed increases in synaptic facilitation support recent findings from biochemical and electrophysiologic studies Indicating presynaptic sites of action contribute to anesthetic-induced depression of excitatory transmission This anesthetic-induced reduction in glutamate release would contribute to the central nervous system depression associated with anesthesia by adding to postsynaptic depressant actions on glutamate receptors.

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Documento generato il 09/04/20 alle ore 05:44:36