Fig. 6.

Modulation of AP dynamics with tonic inhibition within a simplified non–fast-spiking interneuron model. (A) Electrophysiologic features (i), I–F relationship (ii), and ∆ total membrane current (iii) within a simplified non–fast-spiking model and its detailed counterpart (simplified fast-spiking model in SI Appendix, Fig. S6A and parameter values in SI Appendix, Table S2). (B) I_m current generated by the non–fast-spiking model without (gray) and with (blue) tonic inhibition, and impact of changes of I_m current upon gain in this model (SI Appendix, Fig. S6B). (C) Phase-plane and orbits during AP generation of the v–w subsystem of the non–fast-spiking model, with and without tonic inhibition. Yellow denotes bottleneck region. Blue/red asterisks denote AP repolarization and AHP, respectively, corresponding to Inset time–voltage trace. (D) I–F relationship of the v–w system. Despite the absence of an ultraslow (I_m) current, tonic inhibition increases gain. (E) Phase-plane of the v–w system at the bottleneck. Transition from rest to spiking occurs via saddle–homoclinic (S–H) bifurcation (SI Appendix, Fig. S6E). Tonic inhibition reduces activation of w and alters the trajectory through this region. Proportion of total orbit (F) and time (G) spent within bottleneck with increasing input. Despite a similar proportion of the orbit spent within the bottleneck, the presence of tonic inhibition produced faster current–frequency scaling (pink region). This is reflected in a change in the eigenvalue of the unstable manifold of the S–H bifurcation (0.027 and 0.04 without and with tonic inhibition, respectively).