Anti-anxiety drugs reduce conflict-specific “theta”—A possible human anxiety-specific biomarker

Background mes of fear/anxiety are currently ill-defined, with no accepted human biomarkers for anxiety-specific processes. A unique common neural action of different classes of anxiolytic drugs may provide such a biomarker. In rodents, a reduction in low frequency (4–12 Hz; “theta”) brain rhythmicity is produced by all anxiolytics (even those lacking panicolytic or antidepressant action) and not by any non-anxiolytics. This rhythmicity is a key property of the Behavioural Inhibition System (BIS) postulated to be one neural substrate of anxiety. We sought homologous anxiolytic-sensitive changes in human surface EEG rhythmicity. -four healthy volunteers in parallel groups were administered double blind single doses of triazolam 0.25 mg, buspirone 10 mg or placebo 1 hour prior to completing the stop-signal task. Right frontal conflict-specific EEG power (previously shown to correlate with trait anxiety and neuroticism in this task) was extracted as a contrast between trials with balanced approach–avoidance (stop-go) conflict and the average of trials with net approach and net avoidance. s ed with placebo, both triazolam and buspirone decreased right-frontal, 9–10 Hz, conflict-specific-power. tions ne dose of each of only two classes of anxiolytic and no non-anxiolytics were tested, so additional tests are needed to determine generality. sions is a distinct rhythmic system in humans that is sensitive to both classical/GABAergic and novel/serotonergic anxiolytics. This conflict-specific rhythmicity should provide a biomarker, with a strong pre-clinical neuropsychology, for a novel approach to classifying anxiety disorders.