Event-related potentials (ERPs) provide a critical link between the hemodynamic response, as measured by fMRI, and the dynamics of the underlying neuronal activity. Single-trial ERP/EEG recordings capture the oscillatory activity that is hypothesized to underlie both communication between brain regions and amplified processing of behaviorally relevant stimuli. However, precise interpretations of ERPs are precluded by uncertainty about their neural mechanisms. One influential theory holds that averaged sensory ERPs are generated by partial phase resetting of ongoing electroencephalographic oscillations, while another states that ERPs result from stimulus-evoked neural responses. We formulated critical predictions of each theory and tested these using direct, intracortical analyses of neural activity in monkeys. Based a central assumption of "phase resetting" (pre- to post-stimulus phase concentration without increase in power at the dominant frequency of the ERP), evidence from the monkey studies favors a dominant "evoked response" contribution to early components. In further studies, we investigated the homologies between human and simian ERP components, as well as their neural sources in monkeys. We have tracked several ERP components, including C1, P1, N1, MMN and selection negativity down to underlying brain regions, neuronal populations and cellular processes. In sum our findings support a predominant role for stimulus-evoked activity in sensory ERP generation, and make a series of predictions concerning the contributions of phase-resetting to particular ERP components. We also outline both logic and methodology necessary for differentiating evoked and phase resetting contributions to cognitive and motor ERPs in future studies.