PubMed · 11437782
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J A Carter, P McAteer. 2001. Nitrous oxide.. https://doi.org/10.1046/j.1365-2044.2001.02137-23.x
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Whole-cell recordings were made from pyramidal cells visually identified in the CA1 field of adult rat hippocampal slices, and the effects of subanesthetic concentrations of halothane on excitatory postsynaptic currents mediated by non-N-methyl-D-aspartate subtype glutamate receptors were investigated. Halothane concentrations were measured by gas chromatography. At concentrations of 0.2 mM and 0.6 mM, halothane reversibly decreased the amplitude of excitatory postsynaptic currents (EPSCs) evoked by electrical stimulation of Schaffer collateral fibers, and the decrease was accompanied by enhanced paired-pulse facilitation, consistent with the previously reported presynaptic site of halothane's inhibitory action. By contrast, at lower concentrations (0.02 mM and 0.05 mM), halothane increased the amplitude of EPSCs without any appreciable changes in paired-pulse facilitation. Moreover, the frequency of miniature EPSCs arising spontaneously in the presence of tetrodotoxin (mEPSCs) was increased by subanesthetic halothane, but the amplitude of the mEPSCs did not change significantly. These observations suggest that at subanesthetic concentrations halothane postsynaptically enhances glutamatergic excitatory synaptic transmission. This may provide a vital clue to elucidation of the neural mechanisms of the nociceptive reflex enhancement and excitatory state that occur at light levels of anesthesia.
Experiments with volatile agents such as general anesthetics present difficulties in maintaining defined concentrations of these agents during in-vitro experimental conditions. In conventional filtration apparatuses, due to their partition between liquid and vapor phases (to open air or headspaces of the incubation vehicles), some degree of inaccuracy in calculated concentrations of these agents may occur in experiments using these types of chambers. In the present study, a method is described which permits the performance of biochemical experiments in a closed system in which the concentrations of a volatile agent, desflurane, in the liquid phase of the assay environment can be maintained constant for a relatively long time period.
The GABA(A) receptor is an important target for a variety of general anesthetics, including halogenated ethers such as isoflurane and halogenated ethers such as chloroform. Bromoform is a halogenated alkane that exhibits anesthetic properties and has been shown by X-ray crystallography to bind to model anesthetic targets. In this study we report the ability of bromoform to potentiate GABA-induced current in recombinant GABA(A) receptors composed of alpha(1)beta(2)gamma(2s) subunits. Recent studies have shown that specific point mutations in the transmembrane (TM) region of the GABA(A) receptor alpha-subunit can selectively abolish the modulatory activity of specific general anesthetics, and that molecular volume is a key determinant of anesthetic activity. The action of bromoform was examined in a series of mutant receptors and compared with the activity profiles of three other volatile anesthetics. The pharmacological profile of bromoform at the mutant receptors used in this study was similar to that seen with halothane, and distinct from that observed for isoflurane and chloroform. The molecular volume of bromoform is closest to that of halothane, and therefore our data are consistent with the idea that molecular volume is an important determinant of inhaled anesthetic activity at the GABA(A) receptor.