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Lack of Noradrenergic Modulation of Indirect Semantic Priming
Author(s) -
Jacquelyne Cios,
Regan F. Miller,
Ashleigh Hillier,
Madalina E. Tivarus,
David Q. Beversdorf
Publication year - 2009
Publication title -
behavioural neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.859
H-Index - 48
eISSN - 1875-8584
pISSN - 0953-4180
DOI - 10.1155/2009/827101
Subject(s) - lexical decision task , psychology , priming (agriculture) , affect (linguistics) , dopaminergic , semantic memory , norepinephrine , neuroscience , dopamine , cognitive psychology , cognition , communication , biology , botany , germination
Norepinephrine and dopamine are both believed to affect signal-to-noise in the cerebral cortex. Dopaminergic agents appear to modulate semantic networks during indirect semantic priming, but do not appear to affect problem solving dependent on access to semantic networks. Noradrenergic agents, though, do affect semantic network dependent problem solving. We wished to examine whether noradrenergic agents affect indirect semantic priming. Subjects attended three sessions: one each after propranolol (40 mg) (noradrenergic antagonist), ephedrine (25 mg) (noradrenergic agonist), and placebo. During each session, closely related, distantly related, and unrelated pairs were presented. Reaction times for a lexical decision task on the target words (second word in the pair) were recorded. No decrease in indirect semantic priming occurred with ephedrine. Furthermore, across all three drugs, a main effect of semantic relatedness was found, but no main effect of drug, and no drug/semantic relatedness interaction effect. These findings suggest that noradrenergic agents, with these drugs and at these doses, do not affect indirect semantic priming with the potency of dopaminergic drugs at the doses previously studied. In the context of this previous work, this suggests that more automatic processes such as priming and more controlled searches of the lexical and semantic networks such as problem solving may be mediated, at least in part, by distinct mechanisms with differing effects of pharmacological modulation.

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