Fig. 5.
From: Relationship between oxygen consumption and neuronal activity in a defined neural circuit
Systematic correlation between neuronal activity and ventricular O2 levels. a Superior oblique nerve firing rate profile (red trace) of four successive spike bursts (red *) and concurrent alterations of the ventricular O2 concentration (green trace and *) at a ventricular O2 level of ~ 100 μmol/l. b Overlay of spike burst episodes (n = 10) from one preparation and corresponding increases in ventricular O2 consumption (gray traces in the upper and lower plot) along with the respective averages (red and blue traces); vertical dashed line and red arrow indicate the latency of the O2 transient relative to spike burst onset. c Latency of O2 transients (n = 69 from 10 preparations) as function of ventricular O2 concentrations; the slope of the linear regression was not significantly different from zero (r2 = 0.004; p = 0.61). d Integrals of spike bursts and concurrent O2 transients (light red and light green areas in d1, respectively) at a lower (left in d1) and a higher ventricular O2 level (right in d1; green dashed line); d2 shows the dependency of spike burst (red circles) and O2 transient integrals (green circles) on ventricular O2 levels (n = 30 from 10 preparations); note that the integrals of the spike bursts were independent from (red dashed line; r2 = 0.03; p = 0.38), whereas those of the O2 transients significantly increased (green dashed line; r2 = 0.37; p < 0.001) with higher ventricular O2 levels. e, f Dependency of the ratio of O2 consumption and spike burst integral (e; n = 30 from 10 preparations) and of the O2 recovery time (f) from ventricular O2 levels (n = 13 from 6 preparations); note that the slope of the linear regression of the O2/firing rate (e) was significantly different from zero (r2 = 0.14; p < 0.05), whereas that of the O2 recovery (f) was not (r2 = 0.18; p = 0.15). n, number of measurements