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- W2120520440 abstract "Volatile (inhaled) anesthetics cause amnesia at concentrations well below those that cause loss of consciousness and immobility; however, the underlying neuronal mechanisms are unknown. Although many anesthetics increase inhibitory GABAergic synaptic transmission, this effect occurs only at high concentrations (>100 μ m ). Molecular targets for low concentrations of inhaled anesthetics have not been identified. Here, we report that a tonic inhibitory conductance in hippocampal pyramidal neurons generated by α5 subunit-containing GABA A receptors is highly sensitive to low concentrations of the volatile anesthetic isoflurane (ISO) (25 and 83.3 μ m ). The α5 subunit is necessary for enhancement of the tonic current by these low concentrations of isoflurane because potentiation is absent in neurons from α5 -/- mice. Furthermore, ISO (25 μ m ) potentiated recombinant human α5β3γ2L GABA A receptors, whereas this effect was not seen with α1β3γ2L GABA A receptors. These studies suggest that an increased tonic inhibition in the hippocampus may contribute to amnestic properties of volatile anesthetics." @default.
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- W2120520440 date "2004-09-29" @default.
- W2120520440 modified "2023-09-27" @default.
- W2120520440 title "Selective Enhancement of Tonic GABAergic Inhibition in Murine Hippocampal Neurons by Low Concentrations of the Volatile Anesthetic Isoflurane" @default.
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- W2120520440 doi "https://doi.org/10.1523/jneurosci.2063-04.2004" @default.
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