Acute effects of ethanol (0.55 g/kg) and the opioid antagonist naltrex
one (50 mg) on auditory event-related brain potentials (ERP) (i.e., el
ectrical brain activity time-locked to sensory stimuli) were investiga
ted in 13 healthy social drinkers, using a double-blind, placebo-contr
olled, design. The subjects' task was to attend to tones presented to
a designated ear while ignoring tones to the other, and to detect devi
ant tones among the attended tones. When administered alone, naltrexon
e significantly reduced the amplitude of the later part of negative di
fference (Nd-1,), suggesting impaired selective attention. However, th
is effect might have been caused by naltrexone-induced nausea. Ethanol
, when ingested alone, attenuated the amplitude of the NI, and increas
ed the peak latencies of the mismatch negativity (MMN) and N2b that ha
ve been suggested to reflect automatic change detection in audition an
d allocation of attentional resources to processing of stimulus devian
ce, respectively. In contrast, the P1 amplitude was augmented by alcoh
ol, but only when the tones were attended. When ethanol and naltrexone
were simultaneously ingested, however, the alcohol-induced P1 amplitu
de augmentation was canceled, thus tentatively suggesting opioidergic
mediation of this alcohol effect. In contrast, the MMN peak latency wa
s increased significantly more in the interaction condition than in th
e ethanol condition, thus suggesting that the detrimental effects of a
lcohol on involuntary attention switching were augmented by naltrexone
. Furthermore, the N2b amplitude was significantly suppressed in the i
nteraction condition, suggesting attentional impairment. (C) 1998 Else
vier Science Inc.