The effects of general anaesthetics on carbachol-evoked gamma oscillations in the rat hippocampus in vitro
| Autor: | Miles A. Whittington, Nicholas P. Franks, R. Dickinson, William R. Lieb, S. Awaiz |
|---|---|
| Rok vydání: | 2003 |
| Předmět: |
Patch-Clamp Techniques
Carbachol Anesthetics General In Vitro Techniques Inhibitory postsynaptic potential Hippocampus Cellular and Molecular Neuroscience Slice preparation Postsynaptic potential medicine Animals Patch clamp gamma-Aminobutyric Acid Pharmacology Dose-Response Relationship Drug Chemistry GABAA receptor Temperature Excitatory Postsynaptic Potentials Electroencephalography Rats Electrophysiology Solutions Parasympathomimetics Isoflurane Anesthetics Inhalation Biophysics Nerve Net Halothane Neuroscience Anesthetics Intravenous medicine.drug |
| Zdroj: | Neuropharmacology. 44:864-872 |
| ISSN: | 0028-3908 |
| DOI: | 10.1016/s0028-3908(03)00083-2 |
| Popis: | The effects of general anaesthetics and temperature on carbachol-evoked gamma oscillations in the rat hippocampal brain slice preparation were investigated. The frequency of the oscillations was found to be dependent on temperature in the range 32-25 degrees C, with a linear reduction in frequency from 40-17 Hz over this temperature range. The volatile anaesthetics isoflurane and halothane, and the intravenous anaesthetics thiopental, propofol and R(+)-etomidate caused a reduction in the frequency of the oscillations, in a concentration-dependent manner, over a range of clinically relevant concentrations. On the other hand, the intravenous agent ketamine and the "inactive" S(-)-isomer of etomidate had no significant effect on the oscillation frequency. The oscillations were markedly asymmetric over one cycle with a relatively rapid "rising" phase followed by a slower "decaying" phase. The decrease in oscillation frequency was due to an increase in the time-course of the "decaying phase" of the oscillation with little effect on the "rising" phase, consistent with the idea that carbachol-evoked gamma oscillations are trains of GABAergic inhibitory postsynaptic potentials and that the anaesthetics are acting postsynaptically at the GABA(A) receptor. |
| Databáze: | OpenAIRE |
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