Lateralized semantic priming: modulation by levodopa, semantic distance, and participants’ magical beliefs

We tested levodopa effects on lateralized direct and indirect semantic priming in 40 healthy right-handed men in a placebo-controlled, double-blind procedure. Crucially, priming was also analyzed as a function of participants’ positive schizotypal features (magical ideation, MI), previously found to...

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Detalles Bibliográficos
Autores principales: Mohr, Christine, Landis, Theodor, Brugger, Peter
Formato: Texto
Lenguaje:English
Publicado: Dove Medical Press 2006
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2671739/
https://www.ncbi.nlm.nih.gov/pubmed/19412448
Descripción
Sumario:We tested levodopa effects on lateralized direct and indirect semantic priming in 40 healthy right-handed men in a placebo-controlled, double-blind procedure. Crucially, priming was also analyzed as a function of participants’ positive schizotypal features (magical ideation, MI), previously found to be associated with an enhanced semantic spreading activation (SSA) within the right hemisphere. Across both priming conditions, we observed increased semantic priming in the levodopa group 1) specifically after right visual field stimulations and 2) in high MI scorers. In both instances, increased semantic priming emerged from exceedingly long reaction times to unrelated targets reflecting 1) the left hemisphere’s specialization for closely related concepts and 2) an opposite association between MI and SSA in the levodopa as compared with the placebo group. As a final finding, low MI scorers under levodopa performed like high MI scorers under placebo. Our findings speak against a general dopaminergic focusing of SSA, but one that respects each hemisphere’s specialization. They also suggest that individuals’ schizotypal features are important determinants of dopamine-induced changes in hemispheric functioning. We note that, in psychiatric patients, dopamine antagonists reportedly restore unusual lateralization. We discuss this dissociation between schizotypy and schizophrenia as supporting previous notions of protective brain mechanisms operating in the healthy “psychosis-prone” brain.