Volatile and Intravenous Anesthetics Decrease Glutamate Release from Cortical Brain Slices during Anoxia

Bickler, Philip E.; Buck, Leslie T.; Feiner, John

doi:10.1097/00000542-199512000-00014

Cited by 61 publications

(28 citation statements)

References 30 publications

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“…Such inhibition of CNS neuronal Ca channels may contribute to the potential neuroprotective effects of VAs, which have been described in a variety of previous studies and correlate in part to the decrease in cerebral metabolic activity (54)(55)(56)(57). Consistent with these observations are those demonstrating decreased glutamate release from anoxic cortical brain slices in the presence of halothane and enflurane (58) or from the ischemic hippocampal region of rats with isoflurane. It is evident from the tracings that after glutamate release was maximal, the [Ca 2+ ]i continued to increase due to the prolonged K + -induced depolarization.…”

Section: Discussionsupporting

confidence: 68%

Volatile Anesthetic Depression of Ca2+ Entry Into and Glutamate Release from Cultured Cerebellar Granule Neurons

Lynch¹,

Miao²,

Nagao³

et al. 2017

J Anesth Perioper Med

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Section: Discussionsupporting

confidence: 68%

Volatile Anesthetic Depression of Ca2+ Entry Into and Glutamate Release from Cultured Cerebellar Granule Neurons

Lynch¹,

Miao²,

Nagao³

et al. 2017

J Anesth Perioper Med

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“…A number of studies, focusing on the anaesthetic in¯uence on the depolarization-or anoxia-evoked release of neurotransmitters, failed to separate the re-uptake processes from the release itself (Bickler et al, 1995;Eilers & Bickler, 1996;Larsen et al, 1994). The data shown in Figures 1 ± 3 suggest that the re-uptake contribution to reducing the extracellular concentration of neurotransmitters appears to be Figure 3 E ects of the re-uptake inhibitors on the ratios of the second to ®rst K + -evoked glutamate and GABA out¯ow in superfused mouse cerebrocortical slices.…”

Section: Discussionmentioning

confidence: 99%

“…General anaesthetics have been shown to decrease the depolarization-or anoxia-evoked release of glutamate, a major excitatory amino acid in the central nervous system (CNS) (Bickler et al, 1995;Eilers & Bickler, 1996;Liachenko et al, 1998;Miao et al, 1995;Patel et al, 1995;Schlame & Hemmings, 1995). A less predictable behaviour in response to anaesthetics has been found for the inhibitory neurotransmitter, g-aminobutyric acid (GABA).…”

Section: Introductionmentioning

confidence: 99%

Concentration‐dependent isoflurane effects on depolarization‐evoked glutamate and GABA outflows from mouse brain slices

Liachenko

Tang

Somogyi

et al. 1999

British J Pharmacology

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1 The synaptic concentrations of glutamate and g-aminobutyric acid (GABA) are modulated by their release and re-uptake. The e ects of general anaesthetics on these two processes remain unclear. This study evaluates the e ects of iso¯urane, a clinically important anaesthetic, on glutamate and GABA release and re-uptake in superfused mouse cerebrocortical slices. 2 Experiments consisted of two 1.5-min exposures to 40 mM KCl in 30 min intervals. During the second exposure, di erent concentrations of iso¯urane with and without 0.3 mM L-transpyrrolidine-2,4-dicarboxylic acid (PDC, a competitive inhibitor of glutamate uptake transporter) or 1 mM nipecotic acid (a competitive inhibitor of GABA uptake transporter) were introduced. The ratios of the second to ®rst KCl-evoked increases in glutamate and GABA were used to determine the iso¯urane concentration-response curves.3 The results can be described as a sum of two independent processes, corresponding to the inhibitions of release and re-uptake, respectively. The EC 50 values for the inhibitions of release and re-uptake were 295+16 and 805+43 mM for glutamate, and 229+13 and 520+25 mM for GABA, respectively. Addition of PDC did not signi®cantly a ect glutamate release but shifted the re-uptake curve to the left (EC 50 =315+20 mM). Nipecotic acid completely blocked GABA uptake, rendering iso¯urane inhibition of GABA re-uptake undetectable. 4 Our data suggest that iso¯urane inhibits both the release and re-uptake of neurotransmitters and that the inhibitions occur at di erent EC 50 's. For GABA, both EC 50 's are within the clinical concentration range. The net anaesthetic e ect on extracellular concentrations of neurotransmitters, particularly GABA, depends on the competition between inhibition of release and that of re-uptake.

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“…Volatile general anesthetics have been reported previously to have small effects on basal release of glutamate from isolated nerve terminals (synaptosomes) (Hirose et al, 1992;Miao et al, 1995;Schlame and Hemmings, 1995;Westphalen and Hemmings, 2003a) and tissue slices (Bickler et al, 1995;Toner et al, 2001) and of GABA from synaptosomes (Hirose et al, 1992;Mantz et al, 1995;Westphalen and Hemmings, 2003a), which were considered as insignificant. However, even small changes in basal transmitter release may have significant effects on CNS function (Cavelier et al, 2005).…”

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confidence: 99%

Volatile Anesthetic Effects on Glutamate versus GABA Release from Isolated Rat Cortical Nerve Terminals: Basal Release

Westphalen¹,

Hemmings²

2005

J Pharmacol Exp Ther

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The effects of three volatile anesthetics (isoflurane, enflurane, and halothane) on basal release of glutamate and GABA from isolated rat cerebrocortical nerve terminals (synaptosomes) were compared using a dual isotope superfusion method. Concentration-dependent effects on basal release differed between anesthetics and transmitters. Over a range of clinical concentrations (0.5-2ϫ minimum alveolar concentration), basal glutamate release was inhibited by all three anesthetics, whereas basal GABA release was enhanced (isoflurane) or unaffected (enflurane and halothane). These effects may represent a balance of stimulatory and inhibitory mechanisms between transmitters and anesthetics. There were no significant differences between anesthetic effects on basal release in the absence or presence of external Ca 2ϩ , whereas intracellular Ca 2ϩ buffering limited volatile anesthetic inhibition of basal glutamate release. Although these results demonstrate fundamental differences in anesthetic effects on basal release between glutamatergic and GABAergic nerve terminals, all three volatile anesthetics at clinical concentrations consistently reduced the ratio of basal glutamate to GABA release. These actions may contribute to the net depression of glutamatergic excitation and potentiation of GABAergic inhibition characteristic of general anesthesia.

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Volatile and Intravenous Anesthetics Decrease Glutamate Release from Cortical Brain Slices during Anoxia

Abstract: The authors conclude that halothane, enflurane, and sodium thiopental but not propofol, at clinical concentrations, decrease extrasynaptic release of L-glutamate during hypoxic stress.

Cited by 61 publications

References 30 publications

Volatile Anesthetic Depression of Ca2+ Entry Into and Glutamate Release from Cultured Cerebellar Granule Neurons

Volatile Anesthetic Depression of Ca2+ Entry Into and Glutamate Release from Cultured Cerebellar Granule Neurons

Concentration‐dependent isoflurane effects on depolarization‐evoked glutamate and GABA outflows from mouse brain slices

Volatile Anesthetic Effects on Glutamate versus GABA Release from Isolated Rat Cortical Nerve Terminals: Basal Release

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