N-methyl-D-aspartate receptor antagonism impairs sensory gating in the auditory cortex in response to speech stimuli.

Deficits in early auditory sensory processing in schizophrenia have been linked to N-methyl-D-aspartate receptor (NMDAR) hypofunction, but the role of NMDARs in aberrant auditory sensory gating (SG) in this disorder is unclear. This study, conducted in 22 healthy humans, examined the acute effects of a subanesthetic dose of the NMDAR antagonist ketamine on SG as measured electrophysiologically by suppression of the P50 event-related potential (ERP) to the second (S2) relative to the first (S1) of two closely paired (500 ms) identical speech stimuli. Ketamine induced impairment in SG indices at sensor (scalp)-level and at source-level in the auditory cortex (as assessed with eLORETA). Together with preliminary evidence of modest positive associations between impaired gating and dissociative symptoms elicited by ketamine, tentatively support a model of NMDAR hypofunction underlying disturbances in auditory SG in schizophrenia.

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.

EEG correlates of imagery-induced cigarette craving in male and female smokers.

Functional neuroimaging studies of cue-elicited craving in smokers have identified a distributed system of brain activation which includes the frontal cortex. As electroencephalographic (EEG) activity recorded from frontal brain regions indexes emotive functions, which are believed to play a key role in craving processes, this study examined frontal EEG in 20 cigarette smokers (10 male) exposed to imagery scripts containing positive, negative, or neutral affective content with and without descriptions of smoking urges. Urge scripts increased subjective cravings related to both the rewarding and withdrawal-relief properties of smoking, the latter tending to be greater in female smokers, as were self-reports of frustration. The emotional content of scripts did not moderate urges or EEG but urge scripts were found to: a) decrease activity of delta in male smokers and to increase activity of beta, a pattern which has also been seen with acute smoking, and b) increase activity of theta, a response which has also been seen with smoking abstinence. This imagery-elicited neuroelectric profile, appearing to reflect opposing actions of reward and withdrawal, suggests that EEG may be a sensitive tool for probing the multidimensional nature of craving.

Neural effects of nicotine during auditory selective attention in smokers: an event-related potential study.

Acute nicotine has been found to improve task performance in smokers after smoking abstinence, but the attentional processes mediating these improvements are unclear. Since scalp-recorded event-related potentials (ERPs) have been shown to be sensitive indicators of selective attention, the effects of acutely administered nicotine were examined on ERPs and concomitant behavioural performance measures in an auditory selective attention task. Ten (6 males) overnight smoking-abstinent cigarette smokers received nicotine gum (4 mg) in a randomized, double-blind, placebo-controlled, crossover design. In a dichotic listening task [which required participants to attend and detect (target) deviant stimuli in one ear and to ignore similar stimuli in the other ear] which included ERP recordings and assessment of response speed and accuracy measures, nicotine gum failed to alter behavioural performance or amplitudes of ERP components sensitive to selective attention [reflected in the N100 and negative difference (Nd) component] or to pre-attentive detection of acoustic change [reflected in the mismatch negativity (MMN) component]. However, nicotine did influence the speed of these voluntary selective processes, as reflected by shortened latencies of the early Nd component. The findings are discussed in relation to the stimulus filter theory of smoking, and with respect to nicotine's actions on involuntary and controlled aspects of selective attention processes.

Anxiety in rats selectively bred for Fast and Slow kindling rates: situation-specific outcomes.

Rats selectively bred for amygdala excitability, realized by fast or slow kindling epileptogenesis, were previously reported to exhibit differential levels of anxiety. Although the Slow kindling rats generally appeared more anxious in several behavioral tests, under certain test conditions the Fast kindling rats displayed greater anxiety or stressor reactivity. The present investigation confirmed that in a test of anxiety comprising suppression of consumption of a palatable snack in an unfamiliar environment, the Slow kindling rats exhibited greater anxiety and that this effect was attenuated by diazepam. Likewise, the acoustic startle response was greater in the Slow kindling rats. However, the fear-potentiated startle response was more pronounced in Fast kindling rats, particularly among females, irrespective of whether the test parameters elicited moderate or high startle amplitudes. The elevated startle in the Slow rats, and the fear potentiated startle in the Fast rats, were attenuated by diazepam. These data indicate the need to differentiate subtypes of anxiety in animal models, and raise the issue that anxiety elicited by specific environmental triggers may interact with genetically determined trait characteristics.