4.3 Results
4.3.3 Laminar patterns of β -band activity
the proportion ofβ-bursts between error and correct saccade trials in the early post-action period between monkeys (Supplementary Figure 4.2A, early post-action period, adjusted p = 0.116), but foundβ-bursts were significantly more common for both following errors in late post-action period (Supplementary Figure 4.2A, late post-action period, adjusted p<0.001).
Much like we did for trials in which inhibition was successful, we quantified the magnitude of the dif- ference in the p(bursts) between non-canceled and no-stop trials by calculating the effect size at three key epochs: during the fixation, early post-action, and late post-action periods. There were no notable differ- ences between error and correct trials during both fixation and early-action periods. This developed into a medium-to-large effect size during the late post-action period (Figure 4.2F, two-way repeated-measures ANOVA, epoch x control signal, F (1.924, 190.468) = 7349.496, p<0.001). Interestingly, in contrast to canceled trials, β-bursts were equally as common on non-canceled trials and no-stop trials following the feedback tone (Figure 4.2A, Holm post-hoc test, adjusted p<0.001).
To examine if these signals may be used to recruit control in future trials, we determined whether the presence of aβ-burst in the late post-action period on error trials (trial n) influenced the RT on a following no-stop trial (trial n+1). For each channel, we compared the change in RT from non-canceled error trials to no-stop trials, between error trials with aβ-burst present and those without aβ-burst present. Here, negative values represent post-error slowing and positive represents an increase in RT’s following errors. We then calculated the difference in the RT adaptation between those trials with a burst against those without a burst.
This provides a measure of the difference in RT adaptation between burst/no-burst trials. Here positive values represent greater post-error slowing when a burst was observed. In our sample, no channels demonstrated a relationship between bursting and RT adaptation (Figure 4.2G). Thus,β-bursting during the error period is unrelated to RT adaptation.
L2 L3
L5 Cortical Layer L6
0.0 0.5
Normalised power 1.0 Canceled No-stop
SSD SSRT Tone
-6 6
Z-Scored βBDF
L2/3L5/6
200 ms Target
Fixation
Error Tone
A B C 200 ms D
Stopping Post-action
(early) Post-action
(late) Post-action
(early) Post-action (late) 200 ms
Figure 4.3: Laminar properties of intracranialβ-bursts. A. Normalized power in each cortical layer during response inhibition for canceled and latency-matched no-stop trials. The elevation of LFPβ power during response inhibition happened in the deep layers. Conventions as in Figure 4.1.B. Heat maps of LFP β-burst incidence across time and cortical layers on canceled trials during foreperiod (left), stopping and early post-action (left-center), late post-action period (right-center), and error (right) epochs. Yellow represents a greater proportion of (β-bursts) at a given time and depth, relative to other times and depths.
STOP process. We found that normalizedβ-power was significantly greater in L5 & L6 on canceled trials, but not in L2 & L3 (Figure 4.3A, two-way mixed-measures ANOVA, trial type x cortical layer interaction: F (1, 247) = 6.633, p = 0.011). However, we note this effect was driven by one monkey (Supplementary Figure 4.3A).
We then progressed to look at the pattern ofβ-bursts, rather than power, through cortical layers across different functional epochs within our task. We compared the proportion ofβ-bursts observed in each layer during fixation, stopping, early, and late post-action periods on canceled trials, and the late post-action period on noncanceled trials. Although variable at the individual layer level between monkeys, we observed bursting was reliably more prevalent in L3 for both monkeys (Supplementary Figure 4.3B, two-way mixed-measures ANOVA, main effect of cortical layer: F (3, 245) = 27.734, p<0.001).
To examine the temporal profile of this activity, we generated time-depthβ-burst density functions which allow us to see the pattern ofβ-bursts across cortical layers relative to different task events. Given the higher incidence of beta-bursts during these epochs, we examined the laminar pattern of bursts during fixation, stopping, and in the late post-action period on canceled trials, and the early and late post-action period on noncanceled error trials. For each session, this resulted in aβ-burst density function over time and depth which was then z-scored relative to the mean value across all depths and during the entire epoch; higher Z-scores represent a greater proportion ofβ-bursts observed relative to other times and depths. Using this ap- proach, we observed thatβ-bursts were qualitatively more prevalent in upper layers compared to lower layers during fixation, stopping, and errors (Figure 4.3B). This effect was observed in both monkeys (Supplementary Figure 4.3C).
FCz
Upper
Lower
EEGCortical
EEG β-burst
C time
B
0.0 0.2 0.4 0.6 0.8 1.0
p(bursts)
All
EEGIndividual Lower Upper
Fixation Target Post action (early; error)Stopping Tone (error)Post action (late; error)
D
-200 -100 0 100 200
EEG β-burst time - LFP β-burst time (ms) -0.02
0.00 0.02 0.04 0.06
Lower Upper
Observed - shuffled
-1 0 1 2
Area
EEG -> LFP LFP -> EEG
A
EEG
L2
L3 L5
L6
Target Saccade Stop-signal Tone
Signal source
-600 -400 -200 0
Time from target (ms)
200 400 600
Time from error (ms)
-200 0 200 400 600
Time from stop-signal (ms)
-400 -200 0 200
Time from tone (ms) 0
UpperLower
E
Stopping
0 10 20
Odds ratio (OR)
L2/3 x L2/3
L5/6 x L5/6
L2/3 x L5/6 EEG x L2/3
EEG x L5/6
-200 0 200 400 600
Time from stop-signal (ms) Stop-signal
1 Odds ratio (diff)P(sig channels) (diff) 0.1
I J
Fixation Error Stopping Tone
+ve -ve
+ve -ve
Signal A
Signal B
A B
C D
Odds ratio = A D / B C
Coincidental Distinct Trial 1
Trial n
-200 -150
Trial 1
Trial n LFP a
LFP a
-100 -50 0
Bin (ms)
Trial 1
Trial n Signal A (e.g. LFP 1) Signal B
(e.g. LFP 2) A (+ve, +ve) C (+ve, -ve) B (-ve, +ve)
D (-ve, -ve) A (+ve, +ve)
A (+ve, +ve) D (-ve, -ve) D (-ve, -ve)
D (-ve, -ve) C (+ve, -ve) B (-ve, +ve)
B (-ve, +ve) Trial 2
Trial 3
Predictions
Repeated:
(1) for each combination of channels (2) for each time window (3) with shuffled trials for signal B
H
F
G 0Odds ratio25
Low High
L2/3 L5/6
L2/3
L5/6
EEG a = LFP 1
n LFP
a = LFP 1 n LFP
n LFP LFP 1
Adjacent
Upper Lower
EEG Intracortical
Intracortical
0 50
Odds ratio
Figure 4.4:Comparing EEG and intracranialβ-bursts.See footnote2