Fig. 7. Isobolograms for isoflurane (  A ) and halothane (  B ) using network synchronization as the drug effect for combinations of decreases in T-type Ca2+channel conductance and increases in the time constant (τGABAA) governing γ-aminobutyric acid type A (GABAA) receptor deactivation that correspond to the actions of the volatile anesthetics. The isobolograms were generated using the data of  figure 6and the loci of  figure 3to define pharmacologically relevant trajectories. The line emerging from the origin is redrawn from  figure 3, and is the locus of the combined effects of the volatile anesthetic on both the T-type Ca2+channel and GABAAreceptor as volatile anesthetic concentration is increased. For each given volatile anesthetic concentration, the coherence was determined. Isoboles were then generated by connecting this point with points on each axis where modulation of that channel, by itself, would lead to the same network behavior as measured by the coherence. For isoflurane (  A ), isoboles were generated for increments of 0.025 mm on the left and 0.0125 mm on the right. For halothane (  B ), isoboles were generated for increments of 0.04 mm on the left and 0.02 mm on the right. In all panels,  arrows depict the volatile anesthetic concentrations corresponding to minimum alveolar concentration (MAC)-awake. Note the regions of synergy (concave with respect to origin), additivity (linear with respect to origin), and antagonism (convex with respect to origin). Isoboles corresponding to MAC-awake concentrations of isoflurane (  solid lines ) and halothane (  dashed lines ) are depicted in  C . Here, χ2was 0.325 for isoflurane and 0.335 for halothane at MAC-awake. See text for details. 

Fig. 7. Isobolograms for isoflurane (  A ) and halothane (  B ) using network synchronization as the drug effect for combinations of decreases in T-type Ca2+channel conductance and increases in the time constant (τGABAA) governing γ-aminobutyric acid type A (GABAA) receptor deactivation that correspond to the actions of the volatile anesthetics. The isobolograms were generated using the data of  figure 6,and the loci of  figure 3,to define pharmacologically relevant trajectories. The line emerging from the origin is redrawn from  figure 3 , and is the locus of the combined effects of the volatile anesthetic on both the T-type Ca2+channel and GABAAreceptor as volatile anesthetic concentration is increased. For each given volatile anesthetic concentration, the coherence was determined. Isoboles were then generated by connecting this point with points on each axis where modulation of that channel, by itself, would lead to the same network behavior as measured by the coherence. For isoflurane (  A ), isoboles were generated for increments of 0.025 mm on the left and 0.0125 mm on the right. For halothane (  B ), isoboles were generated for increments of 0.04 mm on the left and 0.02 mm on the right. In all panels,  arrows depict the volatile anesthetic concentrations corresponding to minimum alveolar concentration (MAC)-awake. Note the regions of synergy (concave with respect to origin), additivity (linear with respect to origin), and antagonism (convex with respect to origin). Isoboles corresponding to MAC-awake concentrations of isoflurane (  solid lines ) and halothane (  dashed lines ) are depicted in  C . Here, χ2was 0.325 for isoflurane and 0.335 for halothane at MAC-awake. See text for details. 

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