Semantic priming and neurobiology in schizophrenia: A theoretical review

In this theoretical review we bridge the cognitive and neurobiological sciences to shed light on the neurocognitive foundations of the semantic priming effect in schizophrenia. We review and theoretically evaluate the neurotransmitter systems (dopaminergic, GABAergic and glutamatergic) and neurobiological underpinnings of behavioural and electrophysiological (N400) semantic priming in the pathology, and the main hypotheses on their geneses: a disinhibition of the semantic spread of activation, a disorganised semantic storage or noisy lexical-semantic associations, a psychomotor artefact, an artefact of relatedness proportions, or an inability to mobilise contextual information. We further assess the literature on the endophenotype of Formal Thought Disorder from multiple standpoints, ranging from neurophysiology to cognition: considerations are weaved on neuronal (PV basket cell, SST, VIP) and receptor deficits (DRD1, NMDA), neurotransmitter imbalances (dopamine), cortical and dopaminergic lateralisation, inter alia. In conclusion, we put forth novel postulates on the underlying causes of controlled hypopriming, automatic hyperpriming, N400 reversals (larger amplitudes for close associations), indirect versus direct hyperpriming, and the endophenotype of lexical-semantic disturbances in schizophrenia.