| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 9021486 | International Congress Series | 2005 | 4 Pages |
Abstract
The volatile anesthetic, isoflurane, potentiates and inhibits GABAA receptors (GABAARs)function at low and high concentrations, respectively. We examined whether the α subunit isoform influences isoflurane inhibition by studying currents generated by human recombinant α5/1β3γ2L GABAARs. The subunit isoforms selected for the study mediate a tonic (α5) and synaptic (α1) inhibitory conductance in hippocampal pyramidal neurons. The α5 subunit conferred partial resistance to isoflurane blockade compared with the α1 subunit. The steady-state current was preferentially reduced compared with the peak current suggesting that isoflurane inhibited GABAAR function by stabilizing an agonist-bound, closed conformational state or by a use-dependent steric blocking mechanism.
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Authors
B.A. Orser, V.B. Caraiscos, E.K. You-Ten, V.Y. Cheng, J.G. Newell, J.F. MacDonald,