Fig. 2.

ROS homeostasis is linked to neural excitability. (A) ROS and $\partial$ATP levels change with non-spike related cytosolic ATP${}_C$ consumption in our simplified metabolic accounting model. (B) The metabolic signal (MS) as the product of ROS and $\partial$ATP. Two thresholds ${\theta }_{\mathit{RET}}$ (dotted green line) and ${\theta }_{\mathit{FET}}$ (dotted magenta line) control the neural response. (C) Top Panel: Raster of metabolic spikes initiated when the MS $>{\theta }_{\mathit{RET}}$ (black). When Q is low, MS remains higher than ${\theta }_{\mathit{RET}}$ after the refractory period and additional metabolic spiking is initiated (light blue). Lowering the refractory period increases in-burst frequency and decreases inter-burst frequency (dark blue). The Lower panels show the ROS, ATP, and MS levels for 120 ms of the simulation (second, third, and fourth row, respectively) for the three cases. Spikes are marked as “o.” (D) Top Panel: Raster of spikes (gold) in response to an external current source (black). When Q is high such that MS decreases and stays $<{\theta }_{\mathit{FET}}$ for longer (brown) where spiking is prohibited. The Lower panels show the ROS, ATP, and MS level (second, third, and fourth rows). Spikes are marked as “o.” (E and F) The non-spiking related baseline ATP usage (x-axis) and the per-spike-cost Q (y-axis) determine the spectrum of intrinsic firing responses ranging from silent to continuously spiking neurons in RETROS (E) and FETROS (F) conditions.