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Chapter 3
to Bond and Lader (1974)
see supplementary results)
were available for 46 subjects. For each
session we calculated the drug-induced change in prolactin and mood ratings (after - before
drug intake) and compared this with the placebo-induced change [difference score = (drug
session (Time2 –Time1)) – (placebo session (Time2 – Time1))]
(supplementary results:
table S3.1 + mood measures).
Pearson correlations were calculated, in the 10R homozygotes,
between trait anxiety (STAI), trait impulsivity (BIS-11), depression (BDI), listening span
scores, bromocriptine-induced mood changes, bromocriptine-induced prolactin changes and
bromocriptine-induced changes in task switching.
Results
Genetic variation predicts the effect of bromocriptine on task switching
All 48 subjects performed the pre-cued task-switching paradigm after receiving a placebo or
the dopamine receptor agonist bromocriptine (1.25 mg).
Under placebo, there was no difference in terms of task switching between the
DAT1
genotype groups [error rates; Switching x
DAT1
: F(1,46) < 1]. However, consistent with our
0
1
2
3
4
5
6
7
8
9
Drug
Error rate (%): Switch cost (switch - repeat)
placebo bromo-
criptine
bromo-
criptine &
sulpiride
sulpiride
Figure 3.3
Sulpiride abolished the effect of bromocriptine
Shown is the switch cost (switch – repeat) in error rate (percent) for the 10R homozygotes (n = 14)
who received pre-treatment with sulpiride, as well as bromocriptine and sulpiride alone. In this smaller
group, bromocriptine also reduced the switch cost relative to placebo. However, when the same subjects
received sulpiride pre-treatment, bromocriptine no longer facilitated task switching. Error bars represent
the standard error of the difference between switch and repeat trials.