Extracellular Magnesium Ion Modifies the Actions of Volatile Anesthetics in Area CA1 of Rat Hippocampus In Vitro

Rika Sasaki, Koki Hirota, Sheldon H. Roth, Mitsuaki Yamazaki
2002 Anesthesiology  
Magnesium ion (Mg 2؉ ) is involved in important processes as modulation of ion channels, receptors, neurotransmitter release, and cell excitability in the central nervous system. Although extracellular Mg 2؉ concentration ([Mg 2؉ ] o ) can be altered during general anesthesia, there has been no evidence for [Mg 2؉ ] o -dependent modification of anesthetic actions on neural excitability in central nervous system preparations. The purpose of current study was to determine whether the effects of
more » ... er the effects of volatile anesthetics are [Mg 2؉ ] o -dependent in mammalian central nervous system. Methods: Extracellular electrophysiologic recordings from CA1 neurons in rat hippocampal slices were used to investigate the effects of [Mg 2؉ ] o and anesthetics on population spike amplitude and excitatory postsynaptic potential slope. Results: The depression of population spike amplitudes and excitatory postsynaptic potential slopes by volatile anesthetics were significantly dependent on [Mg 2؉ ] o . The effects were attenuated in the presence of a constant [Mg 2؉ ] o /extracellular Ca 2؉ concentration ratio. However, neither N-methyl-D-aspartate receptor antagonists nor a non-N-methyl-D-aspartate receptor antagonist altered the [Mg 2؉ ] o -dependent anesthetic-induced depression of population spikes. Volatile anesthetics produced minimal effects on input-output (excitatory postsynaptic potential-population spike) relations or the threshold for population spike generation. The effects were not modified by changes in [Mg 2؉ ] o . In addition, the population spike amplitudes, elicited via antidromic (nonsynaptic) stimulation, were not influenced by [Mg 2؉ ] o in the presence of volatile anesthetics. Conclusions: These results provide support that alteration of [Mg 2؉ ] o modifies the actions of volatile anesthetics on synaptic transmission and that the effects could be, at least in part, a result of presynaptic Ca 2؉ channel-related mechanisms.
doi:10.1097/00000542-200203000-00026 pmid:11873045 fatcat:ema26ja5hncypp6diqtvzisfii