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Abstract:
Prior experience with a stimulus improves its subsequent
processing. This enhanced efficiency is known as repetition priming
and constitutes a basic learning mechanism, which can be
conceptualized as an expression of rapidly acquired plasticity. In
this study we address the pharmacological modulation of this
plasticity. We tested whether lorazepam and scopolamine would
attenuate behavioural and neural signatures of repetition priming.
Event-related fMRI was combined with psychopharmacology in a word
stem completion paradigm. Participants were given either placebo,
lorazepam (2mg po) or scopolamine (0.4mg iv) prior to testing.
Behaviourally, subjects showed a significant attenuation of
priming, relative to placebo, in both drug groups. In the placebo
group, repetition suppression effects were evident in early visual
regions, in extrastriate/inferior temporal areas, inferior frontal,
middle frontal and dorsal frontal gyrus. In the comparison between
placebo and drug groups, a drug by repetition interaction,
reflecting an absence of repetition suppression in both drug groups
was evident in early visual, inferior temporal and frontal areas.
Even though both drugs impaired repetition suppression, the pattern
of attenuation was different, especially in inferior temporal
cortex. The results suggest that GABAergic and cholinergic systems
influence repetition priming in word stem completion paradigms by
modulation of repetition suppression in task relevant brain areas.
Thus, both drugs modulate neuronal plasticity necessary in basic
learning, as manifest in repetition priming.
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