We have argued that ethanol may produce its effects on micro as well as macro electrophysiology by introducing an increased level of noise or randomness in neuronal processing. Several studies provide data that are descriptively supportive of this idea. For instance, Aston-Jones et al. (1982) demonstrated that low doses of ethanol, although having no effect on the mean spontaneous discharge of rat locus coeruleus neurons, significantly increased the variability in the latency at which those neurons fired in response to sensory stimuli. At the level of the EEG, we have previously demonstrated that consumed ethanol produces increased randomness as indexed by a decrease in the nonlinear structure of EEG oscillations (Ehlers, 1992; Ehlers et al., 1998b). The present study was conducted to further explore that hypothesis by measuring the effects of ethanol on ERO phase synchrony (phase locking) in both humans and animals. We predicted that an ethanol-induced increase in the randomness of neuromolecular interactions would result in a reduction of synchrony or phase locking both within a neuronal population and between neuronal populations. To assess this hypothesis, we explored
