This is the readme for the models associated with the paper: Melnick IV, Santos SF, Safronov BV (2004) Mechanism of spike frequency adaptation in substantia gelatinosa neurones of rat. J Physiol 559:383-95 Abstract: Using tight-seal recordings from rat spinal cord slices, intracellular labelling and computer simulation, we analysed the mechanisms of spike frequency adaptation in substantia gelatinosa (SG) neurones. Adapting-firing neurones (AFNs) generated short bursts of spikes during sustained depolarization and were mostly found in lateral SG. The firing pattern and the shape of single spikes did not change after substitution of Ca2+ with Co2+ , Mg2+ or Cd2+ indicating that Ca2+ -dependent conductances do not contribute to adapting firing. Transient KA current was small and completely inactivated at resting potential suggesting that adapting firing was mainly generated by voltage-gated Na+ and delayed-rectifier K+ (KDR ) currents. Although these currents were similar to those previously described in tonic-firing neurones (TFNs), we found that Na+ and KDR currents were smaller in AFNs. Discharge pattern in TFNs could be reversibly converted into that typical of AFNs in the presence of tetrodotoxin but not tetraethylammonium, suggesting that lower Na+ conductance is more critical for the appearance of firing adaptation. Intracellularly labelled AFNs showed specific morphological features and preserved long extensively branching axons, indicating that smaller Na+ conductance could not result from the axon cut. Computer simulation has further revealed that down-regulation of Na+ conductance represents an effective mechanism for the induction of firing adaptation. It is suggested that the cell-specific regulation of Na+ channel expression can be an important factor underlying the diversity of firing patterns in SG neurones. Although the current simulation does not exactly reproduce Figure 7 from the paper (for some unknown reason), the general result of the paper is supported; the appearance of spike frequency adaptation can be attributed to modulation of Na channels, either through their overall expression (lessening Na channel max conductance gbar_B_Na in the hillock of the model), or shifts in either the activation or inactivation functions of Na channels throughout the neuron. Figure 7: Note the first and fourth columns in figure 7 shows tonic firing with the other columns showing ways to find adaptive firing by the changes mentioned above. Sample explorations of the model: Change gnabar_B_Na in the hillock window to the value 1.8 (S/cm2) Press Init & Run This demonstrates tonic firing. Decreasing gnabar_B_Na to 0.73 then shows only a single spike is generated. Typing at the oc> prompt alpha_shift_B_Na = -3 then restores the tonic firing. Exploring the fifth column by setting gnabar_B_Na = 0.521 S/cm2 at the hillock and typing at the oc> prompt alpha_shift_B_Na = 5 beta_shift_B_Na = 11 and set the current (click the IClamp button and set amp =0.50) Pressing Init & Run then generates a figure like Additional note: In all my models a temperature 6.3 corresponds to a room temperature of 22-24 C, and motoneuron model with 20.3 (6.3 + 14) corresponds to 36-38 C. -Boris Safronov 5/17/2017 Revised by N.T. Carnevale. As noted by the senior author, in the original implementation of this model assigning a value of 6.3 to the parameter "celsius" corresponded to an actual operating temperature of 23 deg C. In this new revision of the model, the value assigned to celsius is identical to the operating temperature, i.e. a value of 23 means 23 deg C. The motivation for the current revision is to facilitate future attributed reuse of this model and the mechanisms that it employs by promoting conceptual clarity and making sure that this code "plays nicely" with other models that involve temperature-dependent mechanisms.