PMID: 8968191Dec 1, 1996Paper

Halothane blocks synaptic excitation of inhibitory interneurons

Anesthesiology
M PerouanskyY Yaari

Abstract

Activation of principal hippocampal neurons is controlled by feedforward and feedback inhibition mediated by gamma-aminobutyric acidergic interneurons. The effects of halothane on glutamate receptor-mediated synaptic excitation of inhibitory interneurons have not been reported yet. The effects of halothane on glutamatergic excitatory postsynaptic currents and on spike threshold in visually identified interneurons were studied with tight-seal, whole-cell voltage- and current-clamp recordings in thin slices from adult mouse hippocampus. The excitatory postsynaptic currents were pharmacologically isolated into their N-methyl-D-aspartate and non-N-methyl-D-aspartate receptor-mediated components using selective antagonists. Halothane (0.37-2.78 mM) reversibly blocked non-N-methyl-D-aspartate and N-methyl-D-aspartate excitatory postsynaptic currents in hippocampal oriens-alveus interneurons. Half-maximal inhibition was observed at similar concentrations (0.59 mM and 0.50 mM, respectively). Halothane inhibited synaptically generated action potentials at concentrations that did not elevate the spike threshold. Halothane blocks glutamate receptor-mediated synaptic activation of inhibitory interneurons in the mouse hippocampus.

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Citations

Oct 2, 1998·British Journal of Pharmacology·E D KirsonM Perouansky
Jul 24, 2001·Anesthesiology·W SimonG Rammes
Dec 29, 1998·IEEE Transactions on Rehabilitation Engineering : a Publication of the IEEE Engineering in Medicine and Biology Society·D B McCreeryM Chatterjee
Feb 11, 2000·Journal of Neurophysiology·K T MoortgatT J Sejnowski

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