Fig. 7. Effects of simulated isoflurane targets on spike latency and Ca²⁺influx. (  A ) Relation between conductance and spike latency, measured as time from stimulus to arrival of the peak of the spike at the bouton, and normalized to the latency of the spike at baseline. All conductances were capable of slowing action potentials. (  A1 ) Reduction of  g^NaV . (  A2 ) Increasing  g^KV . (  A3 ) Increasing  g^KL . (  A4 ) Increasing  g^ClL . (  B ) Effects of conductance changes on spike amplitude. (  B1 ) Inhibition of  g^NaV reduces spike height. (  B2 ) Activation of  g^KV reduces spike amplitude. (  B3 ) Activation of  g^KL causes a small reduction in action potential amplitude. (  B4 ) Activation of  g^ClL increases spike height. (  C ) Relation between conductance and spike breadth, measured as the width at half amplitude (t^1/2). (  C1 ) Reducing  g^NaV causes modest narrowing of action potentials. (  C2 ) Activation of  g^KV strongly reduces t^1/2. (  C3 ) Activation of  g^KL causes a small narrowing of the spike. (  C4 ) Increased  g^ClL causes a slight broadening of the action potential. (  D ) Relation between altered conductances and charge transfer (Q) for Ca²⁺, normalized to baseline conditions and raised to the fourth power (Q^Ca4) to reflect neurotransmitter release. (  D1 ) Reducing  g^NaV causes a monotonic reduction in Q^Ca4. (  D2 ) Increasing  g^KV results in a steep decrease in Q^Ca4. (  D3 ) Increasing  g^KL results in an apparently biphasic response, with a shallow decrease in Q^Cafollowed by a near-linear drop-off. (  D4 ) Activation of  g^ClL causes an inverted U-shaped response, with Q^Caincreasing at low levels, and decreasing toward baseline with higher levels of  g^Cl activation. (  E ) Spike latency versus Q^Ca4. In addition to the conductances shown in panels  A-D above, the results of simulating reduction of  g^KV and  g^CaN are plotted. The relation between latency and Q^Ca4predicts that each conductance should generate a distinct and measurable pattern.