N-methyl-d-aspartate receptor antagonism modulates P300 event-related potentials and associated activity in salience and central executive networks.

Impairments in auditory information processing in schizophrenia as indexed electrophysiologically by P300 deficits during novelty (P3a) and target (P3b) processing are linked to N -methyl- D -aspartate receptor (NMDAR) dysfunction. This study in 14 healthy volunteers examined the effects of a subanesthetic dose of the NMDAR antagonist ketamine on P300 and their relationship to psychomimetic symptoms and cortical source activity (with eLORETA). Ketamine reduced early (e- P3a) and late (l-P3a) novelty P300 at sensor (scalp)-level and at source-level in the salience network. Increases in dissociation symptoms were negatively correlated with ketamine-induced P3b changes, at sensor-level and source-level, in both salience and central executive networks. These P3a alterations during novelty processing, and the symptom-related P3b changes during target processing support a model of NMDAR hypofunction underlying disrupted auditory attention in schizophrenia.

Light up and see: enhancement of the visual mismatch negativity (vMMN) by nicotine.

Both smoking and nicotine can facilitate cognitive efficiency in humans, however the exact mechanism underlying this improvement in cognitive performance is unclear. Nicotine-related improvements in visual task performance may stem from facilitation of the identification and encoding of rare deviant stimuli at early sensory levels. Visual processes at these early levels are thought to be indexed by the visual mismatch negativity (vMMN), an event-related potential (ERP) measure of pre-conscious deviant detection. In order to contribute to our understanding of the neural mechanisms underlying nicotinic modulated cognition, the current study investigated the acute effects of nicotine on vMMN in a non-smoking sample. Twenty-seven volunteers (7 males, 20 females) were treated with nicotine gum (6 mg) in a double-blind randomized, placebo-controlled repeated measures design. ERPs (vMMN; visual N100 and P200) and motor indices of performance were extracted from an intermodal task, requiring participants to attend selectively to auditory targets presented within concurrent, non-overlapping oddball sequences of visual standard and deviant stimuli. Behavioural performance was unaffected by nicotine, however nicotine was found to enhance vMMN and P200 amplitude. The findings are discussed in relation to attentional and neurobiological theories of nicotine dependence and of cognition in general.