title: Amphetamine disrupts P50 suppression in normal subjects.
abstract: BACKGROUND
  P50 suppression is viewed as an operational measure of sensory "gating" that is reduced in patients with schizophrenia and their family members. Previous reports have demonstrated that neural gating is regulated by monoaminergic tone in rodent models of P50 suppression.
  
  
  METHODS
  In this study, 11 healthy subjects participated in P50 event-related potential recordings at baseline and after either oral administration of dextroamphetamine (.3 mg/kg) or placebo, to determine if the administration of a monoaminergic agonist produces P50 suppression deficits similar to those observed in patients with schizophrenia.
  
  
  RESULTS
  As hypothesized, amphetamine disrupted the suppression of the P50 event-related potential. There was a statistically significant decrement in P50 suppression during the amphetamine challenge condition (t10 = 3.15, p < .01, mean difference = -44.1%, d = -2.5) relative to the baseline P50 condition. A comparison of P50 suppression in the placebo and amphetamine conditions (both after a baseline recording session) revealed a significant amphetamine-induced disruption of P50 suppression (t6 = 3.71, p < .01, mean difference = -54.4%, d = -3.14).
  
  
  CONCLUSIONS
  The biochemical alterations associated with an amphetamine-induced disruption of P50 suppression in this study may be related to the pathophysiology of P50 suppression deficits in schizophrenia. The findings are consistent with several careful examinations of suppression deficits in rodent models that have identified the monoaminergic regulation of P50 suppression. These data indicate that amphetamine induces a disruption of P50 suppression in normal subjects.
authors.affiliation: Department of Psychiatry, University of California, San Diego, La Jolla 92093-0804, USA.
authors.forename: G A
authors.initials: GA
authors.lastname: Light
authors.forename: D
authors.initials: D
authors.lastname: Malaspina
authors.forename: M A
authors.initials: MA
authors.lastname: Geyer
authors.forename: B M
authors.initials: BM
authors.lastname: Luber
authors.forename: E A
authors.initials: EA
authors.lastname: Coleman
authors.forename: H A
authors.initials: HA
authors.lastname: Sackeim
authors.forename: D L
authors.initials: DL
authors.lastname: Braff
mesh_terms: D018663:Adrenergic Agents / Q000494:pharmacology*; D000328:Adult; D001143:Arousal / Q000187:drug effects* / Q000502:physiology; D001288:Attention / Q000187:drug effects* / Q000502:physiology; D000697:Central Nervous System Stimulants / Q000494:pharmacology*; D002540:Cerebral Cortex / Q000187:drug effects / Q000503:physiopathology; D003913:Dextroamphetamine / Q000494:pharmacology*; D015259:Dopamine Agents / Q000494:pharmacology*; D004569:Electroencephalography / Q000187:drug effects; D005072:Evoked Potentials, Auditory / Q000187:drug effects* / Q000502:physiology; D006801:Humans; D008297:Male; D012016:Reference Values; D012559:Schizophrenia / Q000503:physiopathology
chemical_list: D018663:Adrenergic Agents; D000697:Central Nervous System Stimulants; D015259:Dopamine Agents; D003913:Dextroamphetamine