title: Anti-anxiety drugs reduce conflict-specific "theta"--a possible human anxiety-specific biomarker.
abstract: BACKGROUND
  Syndromes 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.
  
  
  METHODS
  Thirty-four healthy volunteers in parallel groups were administered double blind single doses of triazolam 0.25mg, buspirone 10mg 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.
  
  
  RESULTS
  Compared with placebo, both triazolam and buspirone decreased right-frontal, 9-10 Hz, conflict-specific-power.
  
  
  CONCLUSIONS
  Only one dose of each of only two classes of anxiolytic and no non-anxiolytics were tested, so additional tests are needed to determine generality.
  
  
  CONCLUSIONS
  There 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.
authors.affiliation: Department of Psychology and Department of Psychological Medicine, University of Otago, POB56, Dunedin 9054, New Zealand. nmcn@psy.otago.ac.nz
authors.forename: Neil
authors.initials: N
authors.lastname: McNaughton
authors.forename: Charles
authors.initials: C
authors.lastname: Swart
authors.forename: Phoebe
authors.initials: P
authors.lastname: Neo
authors.forename: Vanessa
authors.initials: V
authors.lastname: Bates
authors.forename: Paul
authors.initials: P
authors.lastname: Glue
mesh_terms: D000293:Adolescent; D000328:Adult; D014151:Anti-Anxiety Agents / Q000494:pharmacology*; D001007:Anxiety / Q000503:physiopathology / Q000517:prevention & control*; D015415:Biomarkers; D001921:Brain / Q000187:drug effects* / Q000502:physiology; D002065:Buspirone / Q000494:pharmacology*; D003220:Conflict, Psychological; D004311:Double-Blind Method; D004569:Electroencephalography; D005260:Female; D006801:Humans; D008297:Male; D014229:Triazolam / Q000494:pharmacology*; D055815:Young Adult
chemical_list: D014151:Anti-Anxiety Agents; D015415:Biomarkers; D014229:Triazolam; D002065:Buspirone