Moeller SJ Supplementary 1
SUPPLEMENTARY MATERIALS AND METHODS
Subjects
Subjects from both samples were recruited using advertisements in local newspapers, by word-of
mouth, and from local treatment facilities. All were fully informed of all study procedures and
risks, and provided written consent in accordance with the local Institutional Review Board.
Subjects were healthy and free of medications, as ascertained during a full physical and
neurological examination by a neurologist and a diagnostic interview by a clinical psychologist.
This interview included the Structured Clinical Interview for DSM-IV Axis I Disorders [research
version1, 2], the Addiction Severity Index3, the Cocaine Selective Severity Assessment Scale4 and
the Cocaine Craving Questionnaire5. Exclusion criteria were as follows: (A) history of head
trauma or loss of consciousness (> 30 min) or other neurological disease of central origin
(including seizures); (B) abnormal vital signs at time of screening; (C) history of major medical
conditions, encompassing cardiovascular (including high blood pressure, cardiac arrhythmias
apart from sinus bradycardia, or an abnormal electrocardiography at time of screening),
endocrinological (including metabolic), oncological, or autoimmune diseases; (D) history of
major psychiatric disorder (other than substance abuse or dependence for the cocaine subjects
and/or nicotine dependence for both groups); (E) pregnancy as confirmed with a urine test in all
female subjects; (F) contraindications to the MRI environment; and (G) except for cocaine in the
cocaine subjects, positive urine screens for psychoactive drugs or their metabolites
(amphetamine/methamphetamine,
phencyclidine,
benzodiazepines,
cannabis,
opiates,
barbiturates and inhalants). For Sample 2, history of glaucoma was added as an additional
exclusionary criterion because of methylphenidate administration.
Moeller SJ Supplementary 2
Sample 1 comorbidities were as follows: one subject also met criteria for current
marijuana dependence, and 23 cocaine subjects were current cigarette smokers. Past
comorbidities were identified in 25 cocaine subjects and included fully sustained remission for
alcohol (N=18), marijuana (N=11), opioid (N=1), hallucinogen (N=1), other stimulant (N=1) or
polysubstance (N=2) use disorders. Sample 2 comorbidities were as follows: one cocaine subject
also met criteria for current heroin dependence, and 10 cocaine subjects were current cigarette
smokers. Comorbidities in remission among the cocaine subjects included alcohol (N=8) and
marijuana (N=6) use disorders.
Task Training
Just before the fMRI task, subjects completed extensive training to decrease performance
differences between the groups. Training consisted of at least two complete task runs with
different color randomizations, once outside and once inside the scanner (one Sample 1 cocaine
subject did not perform the training inside the scanner). After training, all subjects had achieved
accuracies of ≥ 50%.
Calculation of Post-Conflict and Post-Error Slowing
Post-conflict slowing was calculated as ([iC+cI] – [cC+iI], where iC=congruent trial preceded by
an incongruent trial, cI=incongruent trial preceded by a congruent trial, etc.; note the iI were null
events, as in our task the incongruent events did not occur back-to-back) and post-error slowing
(i.e., comparing RT for trials after errors versus RT for trials after correct responses)6. Following
established procedures6, for the post-conflict slowing we excluded trials with an exact stimulus
repetition (in color, word, or both) across consecutive trials, which could artifactually influence
post-conflict slowing scores7. For post-error slowing, we calculated three scores: (A) slowing
after an error when the current trial is a congruent event, (B) slowing after an error when the
Moeller SJ Supplementary 3
current trial is an incongruent event, and (C) their sum. Post-error slowing is an adaptive,
corrective response that is thought to enable more controlled responding to prevent future errors8,
9
.
Task-Related Ratings (Sample 1 Only)
To bolster the case for fatigue, we further examined task-related ratings that were obtained while
these same Sample 1 subjects performed a drug Stroop task, which has been extensively
described elsewhere10-13. All subjects performed the drug Stroop task before the color word
Stroop task (drug Stroop data are not presented here). In particular, we inspected self-reported
ratings of ‘sleepiness’ (a proxy for fatigue) (‘‘how sleepy are you right now?’’) (response scale:
not at all to very much, 0 to 10) and parallel ratings for ‘interest’ (a proxy for vigilance and
attention) (‘‘how interested are you in the task right now?’’) (same response scale). To obtain a
measure of how much fatigue (or interest) increased during this drug Stroop task, we subtracted
sleepiness ratings collected at the beginning of the drug Stroop task from the sleepiness ratings
collected at the end of this task (the latter rating collected immediately before beginning the
color word Stroop task). Both ratings were obtained using custom programs written in C++ and
were presented through MRI compatible goggles.
Methylphenidate Procedures (Sample 2 only)
During two fMRI scanning sessions on two separate study days, oral methylphenidate (20 mg) or
placebo (lactose) was administered in a counterbalanced fashion across all subjects (note that
there were no differences between the groups in number of days between the methylphenidate
and placebo scans (cocaine: 8.82.9; control: 20.416.8; P>0.1). Oral methylphenidate or
placebo was given 90 minutes prior to completion of the color word Stroop task, within the
window of its peak effects (60-120 minutes)14. Measures of cardiovascular functioning (heart
Moeller SJ Supplementary 4
rate, blood pressure) and self-reports of methylphenidate effects were collected throughout the
study. Heart rate was monitored at baseline (pre-medication), 45 min post-medication, 120 min
post-medication, and post-fMRI as part of medical clearance. Blood pressure was taken at
baseline and post-fMRI (in conjunction with the first and fourth heart rate measurements).
Subjects also completed the Profile of Mood States, for which they provided self-report ratings
(0-10, “How do you feel right now?”) for the dimensions of “high” and “methylphenidate
desire.” These self-report measures were collected pre-medication, 45 min post-medication, and
120 min post-medication. Results of these measures are reported elsewhere15, showing that this
oral dose of methylphenidate does not increase craving in cocaine subjects.
To comprehensively monitor the stimulant effects of methylphenidate (i.e., elevated
cardiovascular reactivity, of special concern to a cocaine addicted population), study personnel
were not blinded to the administered challenge during running of most subjects (N=25). Once it
became clear that risks were minimal, we transitioned to double-blind MPH administration (N=4,
two of whom were controls). However, even with single-blind administration, there were no
differences between study days in post-fMRI guesses for the medication received (guess
methylphenidate vs. placebo; χ2(1)=0.0, P>0.6), indicating that subjects were not fully aware of
the exact type of medication received. Thus, we included these four subjects to maximize the
number of subjects available for analysis. We also accounted for potential effects of single-blind
versus double-blind medication administration as described below.
Covariate Analyses
SPSS analyses were used to control for variables that differed between the groups (Table 1, main
text). For these covariate analyses, we inspected associations between the respective covariate
and our dependent variables of interest [regions of interest (ROIs), behavioral measures]; if
Moeller SJ Supplementary 5
significantly correlated across all study subjects (P<0.05), these variables were entered as
covariates in the relevant SPSS ANOVA or as control variables in partial correlations as
appropriate16. All continuous and normally distributed variables were inspected with parametric
tests (within groups: paired t-test; between groups: independent t-tests; correlations: Pearson r).
Variables that were not normally distributed were inspected with the respective non-parametric
tests (Wilcoxon, Mann-Whitney U, or Spearman r).
SUPPLEMENTAL RESULTS
Sample 1: Additional Behavior
Given our central interest in the neural response to error, in addition to the analyses described in
the main text we performed a 2 (repetition) × 2 (congruency) × 2 (correctness) × 2 (group) mixed
ANOVA for RT. This analysis revealed only a main effect of congruency as expected (P<0.001);
no main effects or interactions were observed for correctness (i.e., RT for error trials versus RT
for correct trials) (F<2.1, P>0.1). Thus, it is unlikely that the fMRI effects reported in the main
text are attributable to differences in RT.
Although post-error slowing previously has been linked to adaptive, top-down control8, 9,
we nonetheless endeavored to link it to task performance in the current study. Because the
overall number of errors was not large (see Table 1, main text) – meaning it was not feasible to
analyze back-to-back errors in this sample – we tested for correlations between post-error
slowing with RT and task performance across the task. In the cocaine subjects only, there was a
trend for those who showed the greatest increase in task errors (fourth repetition>first repetition)
to also show the greatest decrease in respective post-error slowing (r=-0.48, P<0.05). Because
this effect did not meet the nominal P<0.01 significance level established for correlations in this
Moeller SJ Supplementary 6
study, effects of post-error slowing in the current study should be interpreted with caution as also
indicated in the main text.
Sample 1: Additional SPM
Across task repetitions and groups, and for both the ‘congruency’ and ‘correctness’ main effect
contrasts, there were significant activations in multiple brain regions previously reported to be
engaged by the color-word Stroop task6,
17
(Figure S1A-B). Such results contribute to a long-
standing effort of using the color-word Stroop task to interrogate the prefrontal cortex in a range
of subject populations that include healthy controls18, stimulant dependent populations19,
schizophrenia patients20, and even relatives of affected probands21.
Sample 1: Effects of Covariates
Covarying out smoking history, which differed between the study groups (Table 1, main text),
did not attenuate the post-error slowing repetition main effect or repetition × group interaction
(P<0.05), the dACC repetition main effect (P<0.01), or the midbrain repetition × group
interaction (P<0.01). The latter suggests that our results cannot be attributed to the desensitizing
effects of cigarette smoking on midbrain dopamine neurons22. Covarying out age, which also
differed between the groups (Table 1), did not attenuate the post-error slowing main effect of
repetition (P<0.05) or the midbrain repetition × group interaction (P<0.001); however, covarying
out age did attenuate the post-error slowing repetition × group interaction (P>0.07). Other effects
did not require covariate analyses, as they were not associated with cigarette smoking or age16. In
addition, note that the midbrain repetition × group interaction remained significant when
dividing the cocaine subjects into those testing positive or negative for cocaine in urine23, 24, or
when dividing the cocaine subjects into those with or without current cocaine dependence (with
the latter encompassing cocaine abuse, remission, and polysubstance abuse; see above).
Moeller SJ Supplementary 7
Sample 1: Effects of Second and Third Repetitions
Here we reanalyzed our main results from the main text (increased errors, decreased post-error
slowing, decreased dACC activity to error, repetition × group interaction in the midbrain) while
also including the second and third task repetitions, therefore testing for graded effects as a
function of time-on-task.
Errors
For task errors, we expected significant repetition-related increases (Repetition 1 < Repetition 2
< Repetition 3 < Repetition 4) across all subjects. Consistent with hypotheses, the linear contrast
was significant across the congruent and incongruent trials, and across all subjects, indicating
that subjects committed progressively more errors throughout the task [F(1,51)=20.0, P<0.001].
There was also a congruency × repetition linear contrast interaction [F(1,51)=22.0, P<0.001],
such that this linear increase in errors was significant only during the congruent trials
[F(1,51)=21.8, P<0.001] (Figure S2A). In addition to supporting the effects above, this finding
again speaks against alternative explanations of our results (e.g., practice effects).
Post-Error Slowing
For post-error slowing, we expected a repetition × group interaction, such that repetition-related
decreases (Repetition 1 > Repetition 2 > Repetition 3 > Repetition 4) would be more pronounced
in the healthy control subjects. Consistent with hypotheses, the linear contrast was significant for
the repetition × group interaction [F(1,41)=7.9, P<0.01]. In particular, the descending linear
contrast was significant only in controls [F(1,17)=16.9, P<0.01] (Figure S2B), indicating that
only this group progressively decreased their post-error slowing throughout the task (although
inspection of the means indicates a possible floor effect in the cocaine subjects).
SPM
Moeller SJ Supplementary 8
To examine all four repetitions in the dACC/supplementary motor area and midbrain, we
estimated a 4 (repetition: first, second, third, fourth) × 2 (group: control, cocaine) mixed
ANOVA in SPM. Analyzing all repetitions resulted in 27/33 cocaine subjects and 14/20 controls
included in this model. We then extracted the error-induced BOLD signal in the same peak
coordinates in the dACC/supplementary motor area and midbrain that were found for the main
analyses (i.e., those that emerged when analyzing the first and last task repetitions; see Table 2,
main text, for peak coordinates) for subsequent analysis in SPSS.
dACC. For the dACC, we expected significant repetition-related activation decreases (Repetition
1 > Repetition 2 > Repetition 3 > Repetition 4) across all subjects. Consistent with hypotheses,
the
descending
linear
contrast
was
significant
across
all
subjects
for
all
three
dACC/supplementary motor area peak coordinates [Fs(1,39)>8.4, P<0.01] (Figure S2C). These
results indicate that activity in the dACC (and supplementary motor area) progressively
decreased with repetition throughout the task in all subjects, further buttressing the idea of
mental fatigue (which occurred in a graded fashion as a function of time-on-task).
Midbrain. For the midbrain, we expected a repetition × group interaction, such that repetitionrelated activation decreases would emerge in the cocaine subjects, while repetition-related
activation increases (Repetition 1 < Repetition 2 < Repetition 3 < Repetition 4) would emerge in
controls. Indeed, the repetition × group linear contrast interaction in the midbrain was significant
[F(1,39)=9.4, P<0.01], such that the cocaine subjects progressively decreased response in this
region with repetition as hypothesized [F(1,26)=16.3, P<0.001] (Figure S2D). Although the
healthy controls did not progressively increase response in this region with repetition
[F(1,13)=0.8, P>0.3), the significant omnibus interaction directly supports the findings for the
first and last task repetition.
Moeller SJ Supplementary 9
Sample 2: Behavior
Because methylphenidate previously has been shown to facilitate task performance in cocaine
addicted individuals15, 25 and even in healthy controls15, here we tested its impact on performance
of the color word Stroop task. We were specifically interested in testing for methylphenidate
modulation of task repetition effects [note that main effects of methylphenidate (i.e., collapsed
across all task conditions and repetitions) will be reported separately].
Behavioral data (errors, RT, and post-error slowing on congruent trials) were (separately)
analyzed with 2 (medication: methylphenidate, placebo)  2 (repetition: first, third)  2
(congruency: congruent, incongruent) × 2 (group: cocaine, control) ANOVAs. In support of the
main effect of repetition on post-error slowing above, there was a similar trend in this smaller
sample (first>third: F1,17=3.6, P<0.08). In contrast, errors showed a unique pattern, such that the
four-way interaction was significant (F1,23=4.3, P<0.05): only during the more prevalent
congruent trials, placebo was associated with the expected decline in task performance (more
errors) with repetition in controls but not in cocaine subjects; moreover, the opposite pattern of
results for both groups emerged during methylphenidate. However, because this four-way
interaction did not survive correction for covariates (see below), and did not approach
significance when including all three repetitions (P>0.2), it requires replication in future studies
with larger samples and is not further interpreted. There were main effects of congruency for the
absolute number of errors (congruent trials>incongruent trials, P<0.001, again likely due to the
higher number of congruent trials) and RT (incongruent trials>congruent trials, P<0.001), both
consistent with the effects in Sample 1. There were no additional effects for RT (P>0.05).
Sample 2: Additional SPM
Moeller SJ Supplementary 10
Across task repetitions, medications, and groups, similar activation patterns to Sample 1 were
observed in Sample 2 during both conflict and error trials (Figure S1C-D). Consistent with the
results from Sample 1, there were no significant activations for the ‘correctness × congruency’
interaction contrast.
Inspection of the Locus Coeruleus
Because methylphenidate also acts on noradrenergic systems, and because our midbrain peak
coordinate was located near the locus coeruleus, here we tested whether an ROI analysis of this
region would reveal a significant way repetition × medication × group interaction. We created a
bilateral 10 mm spherical mask around the locus coeruleus, taken from peak coordinates from a
previous study26. SPM analysis was conducted using the same models as described in the main
text. Similarly to our other ROI analysis with the midbrain (main text), SPM analyses were
conducted using a search threshold of P<0.05 voxel-level corrected (extent of 15 voxels). The
three-way interaction was not significant, speaking against a primary role of norepinephrine in
the current findings (note that nonsignificant effects of this same locus coeruleus mask were
likewise observed for the repetition × group interaction in Study 1).
Sample 2: Effects of Covariates
Covarying out age, depression, or smoking history, all of which differed between the study
groups (Table 1, main text), did not attenuate the three-way repetition × medication × group
interaction in the midbrain (P<0.05). Similarly, including double-blind versus single blind
medication administration as a dummy covariate did not attenuate the three-way interaction in
the midbrain (P<0.001). The latter result justifies inclusion of all 29 subjects. The four-way
medication  repetition  congruency × group behavioral interaction for errors did not survive
correction for age (P>0.1).
Moeller SJ Supplementary 11
Sample 2: Effects of Third Task Repetition
We tested the repetition × medication × group interaction in the midbrain while also including
the second task repetition. We included subjects who had usable scans from 5/6 task conditions
(2 medications × 3 repetitions), resulting in 13/14 cocaine subjects and 11/15 controls in the
analysis. A 3 (repetition: first, second, third) × 2 (medication: methylphenidate, placebo) × 2
(group: control, cocaine) mixed ANOVA in SPM was estimated for this purpose. We predicted a
three-way interaction. The same pattern of linear contrasts was expected for placebo as described
above for Sample 1: repetition-related activation decreases in the cocaine subjects (Repetition 1
> Repetition 2 > Repetition 3), but repetition-related activation increases in controls (Repetition
1 < Repetition 2 < Repetition 3 < Repetition 4). The opposite pattern of linear contrasts was
expected during methylphenidate. We again extracted the error-induced BOLD signal in the
same midbrain peak coordinates that were found for the main analyses for subsequent analysis in
SPSS.
Results supported our hypotheses, revealing a significant three-way linear contrast
interaction [F(1,11)=16.2, P<0.01]. During placebo, linear contrasts did not reach significance in
either study group (P>0.1), although both study groups showed patterns of results in the
hypothesized directions (Figure S3B). Importantly, during methylphenidate, the cocaine subjects
showed progressively increased midbrain activity with repetition [F(1,10)=10.5, P<0.01],
whereas the controls showed progressively decreased midbrain activity with repetition
[F(1,5)=9.3, P<0.05] (Figure S3A).
Moeller SJ Supplementary 12
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Moeller SJ Supplementary 15
Supplementary Figure Legends
Figure S1. Task activations across all subjects and conditions, split by Sample (A-B: Sample 1;
C-D: Sample 2) and task events (conflict: A, C; error: B, D). Activations are thresholded at
whole-brain PFWE<0.05 (family-wise error correction, 15 contiguous voxels). Note that no task
activations were significant at this corrected threshold for the correctness × congruency
interaction, for either Sample 1 or Sample 2.
Figure S2. Sample 1 effects when including all four task repetitions. During the event-related
color-word Stroop task, there were (A) progressively more congruent errors in all subjects and
(B) progressively less post-error slowing (when the current trial was a congruent event) in
controls. (C) There was also progressively less % BOLD signal change to error (compared with
all correct trials) in the dorsal anterior cingulate cortex (dACC) in all subjects. (D) Finally, there
was progressively less % BOLD signal change to error (compared with all correct trials) in the
midbrain in the cocaine subjects, but not in controls. Asterisks denote repetition linear contrasts
that are significant in only one study group (P<0.05).
Figure S3. Sample 2 three-way medication × repetition × group interaction in the midbrain when
including all three task repetitions. (A) During methylphenidate, there was progressively more
midbrain response to error in the cocaine subjects, but progressively less in the control subjects.
(B) An opposite (but nonsignificant) pattern of results was observed during placebo. Asterisks
denote significant repetition linear contrasts (P<0.05).
Moeller SJ Supplementary 16
Table S1. Performance on the color-word Stroop fMRI task across all Sample 1 study subjects
(33 cocaine subjects, 20 healthy controls).
First task repetition
Percent Accuracy
Congruent
Incongruent
(Incongruent – congruent)
# Errors2
Congruent
Incongruent
(Incongruent – congruent)
Reaction time, all trials (msec)
Congruent
Incongruent
(Incongruent – congruent)
Reaction time, correct trials only (msec)
Congruent
Incongruent
(Incongruent – congruent)
Post-conflict slowing
Post-error slowing: congruent trials1
Last task repetition
Percent Accuracy
Congruent
Incongruent
(Incongruent – congruent)
# Errors
Congruent
Incongruent
(Incongruent – congruent)
Reaction time, all trials (msec)
Congruent
Incongruent
(Incongruent – congruent)
Reaction time, correct trials only (msec)
Congruent
Incongruent
(Incongruent – congruent)
Post-conflict slowing
Post-error slowing: congruent trials1
t
Cocaine
N=33
Control
N = 20
0.3
1.3
1.6
.94  .01
.59  .05
-.35  .04
.93  .02
.69  .05
-.24  .04
0.3
1.3
0.7
11.8  2.1
4.9  0.6
-6.9  1.8
12.9  3.2
3.7  0.6
-9.2  3.0
0.3
1.1
1.1
685.5  10.9
902.7  15.6
217.2  15.0
681.1  12.6
874.5  19.7
193.4  22.3
0.1
0.7
0.6
1.3
2.3*
686.1  11.0
904.1  19.4
218.1  16.1
932.5  21.8
41.9  15.2
683.5  13.6
885.0  20.1
201.5  21.3
885. 4  27.4
91.7  11.8
0.1
1.5
1.8
.89  .02
.58  .04
-.31  .04
.89  .02
.68  .05
-.21  .04
0.1
1.5
0.3
19.9  3.1
5.0  0.5
-14.9  2.9
20.3  4.5
3.9  0.6
-16.4  4.1
0.5
2.4*
2.2*
692.6  10.0
912.7  16.0
220.2  14.7
685.1  13.1
848.2  22.8
163.1  22.8
0.2
1.5
1.5
1.4
0.5
693.7  10.3
918.0  16.9
224.3  16.5
946.9  19.8
26.3  17.5
687.1  13.6
869.2  23.3
182.1  22.1
896.1  31.3
14.7  12.5
Note. Values are means  standard error of the mean (SEM). *P<0.05; 1Data missing for one
control, and three cocaine subjects; 2For errors, a seemingly unexpected main effect of
congruency [congruent errors>incongruent errors: F(1,51)=37.8, P<0.001] is explained by the
higher number of congruent trials than incongruent trials, thus providing more opportunities for
errors to be committed during the former; indeed, a subsequent analysis of percent accuracy
revealed the reliable Stroop interference effect [congruent percent accuracy>incongruent
percent accuracy: F(1,51)=109.0, P<0.001], but there were no repetition effects.
SPM mip
[0, 18, 4
SPM mip
[6, 15, 48
20
<
SPM{T51}
20
SPM{T }
40
40
51
Moeller
SJ Supplementary
17
<
60
60
80
Fig
S1.
SPMresults:
.\ANOVA33SDI&20C_BI_BC
Height threshold T = 5.10
Extent threshold k = 5 voxels
Height threshold T = 5.10
Extent threshold k = 5 voxels
100
10
A.
20 30 40
Design matrix
100
10
50
activ
<
<
contrast(s)
<
contrast(s)
SPM mip
[6, 21, 42]
SPM mip
[6, 18, 51]
2
6
15
10
20
<
SPM{T69}
20 30 40
Design matrix
B.
activ
<
80
SPMresults: .\ANOVA33SDI&20C_WB_CB
10
20
5
40
SPM{T69}
<
0 60
0
Height threshold T = 4.93
Extent threshold k = 5 voxels
10
15
20
30
Design matrix
100
10
D.
12
10
10
8
6
5
4
2
0
60
SPMresults: .\ColorWord_Motivation_MPH_14CUD&15Control_3cond_WB_CB
100
C.
40
80
80
SPMresults: .\ColorWord_Motivation_MPH_14CUD&15Control_3cond_BI_BC
Height threshold T = 4.93
Extent threshold k = 5 voxels
5
0
20
30
Design matrix
50
Moeller SJ Supplementary 18
Fig S2.
B.
30
25
120
Linear (All Subjects): P<0.001
Post-Error Slowing
(msec) (Congruent)
Total Errors (Congruent)
A.
20
15
10
5
0
80
60
40
20
0
-20
Cocaine
Cocaine
Linear (Interaction): P<0.01
Control
Cocaine
Cocaine
Control
Repetition 1
Repetition 3
Repetition 2
Repetition 4
Control
Control
D.
1
0.5
0
Linear (All Subjects): P<0.01
-0.5
Cocaine
Cocaine
Control
Control
% BOLD Signal Change:
Midbrain: x=6, y=-18, z=-9
C.
% BOLD Signal Change:
dACC: x=6, y=12, z=45
*
100
1
*
0.5
0
Linear (Interaction): P<0.01
-0.5
Cocaine
Cocaine
Control
Control
Moeller SJ Supplementary 19
Fig S3.
A.
B.
Placebo
1.5
1
*
*
0.5
Repetition 1
0
Repetition 2
-0.5
Repetition 3
-1
% BOLD Signal Change:
Midbrain: x=-3, y=-18, z=-15
% BOLD Signal Change:
Midbrain: x=-3, y=-18, z=-15
Methylphenidate
1.5
1
0.5
0
-0.5
-1
-1.5
-1.5
Cocaine
Cocaine
Control
Control
Cocaine
Cocaine
Control
Control