The current review constitutes the first comprehensive look at the possibility that the mismatch negativity (MMN, the deflection of the auditory ERP/ERF elicited by stimulus change) might be generated by so-called fresh-afferent neuronal activity. This possibility has been repeatedly ruled out for the past 30 years, with the prevailing theoretical accounts relying on a memory-based explanation instead. We propose that the MMN is, in essence, a latency-and amplitude-modulated expression of the auditory N1 response, generated by fresh-afferent activity of cortical neurons that are under nonuniform levels of adaptation.

Being able to detect unusual, possibly dangerous events in the environment is a fundamental ability that helps ensure the survival of biological organisms. Novelty detection requires a memory system that models (builds neural representations of) events in the environment, so that changes are detected because they violate the predictions of the model. The earliest physiologically measurable brain response to novel auditory stimuli is the mismatch negativity, MMN, a component of the event-related potential. It is elicited when a predictable series of unvarying stimuli is unexpectedly followed by a deviating stimulus. As the occurrence of MMN is not usually affected by the direction of attention, MMN reflects the operation of automatic sensory (echoic) memory, the earliest memory system that builds traces of the acoustic environment against which new stimuli can be compared. The dependence of attentive novelty detection on earlier, pre-attentive processes, however, has remained elusive. Previous, related studies seem to suggest a relationship between MMN and attentive processes, although no conclusive evidence has so far been shown. Here we address novelty detection in humans both on a physiological and behavioural level, and show how attentive novelty detection is governed by a pre-attentive sensory memory mechanism.

Life or death in hostile environments depends crucially on one's ability to detect and gate novel sounds to awareness, such as that of a twig cracking under the paw of a stalking predator in a noisy jungle. Two distinct auditory cortex processes have been thought to underlie this phenomenon: (i) attenuation of the so-called N1 response with repeated stimulation and (ii) elicitation of a mismatch negativity response (MMN) by changes in repetitive aspects of auditory stimulation. This division has been based on previous studies suggesting that, unlike for the N1, repetitive ''standard'' stimuli preceding a physically different ''novel'' stimulus constitute a prerequisite to MMN elicitation, and that the source loci of MMN and N1 are different. Contradicting these findings, our combined electromagnetic, hemodynamic, and psychophysical data indicate that the MMN is generated as a result of differential adaptation of anterior and posterior auditory cortex N1 sources by preceding auditory stimulation. Early (Ϸ85 ms) neural activity within posterior auditory cortex is adapted as sound novelty decreases. This alters the center of gravity of electromagnetic N1 source activity, creating an illusory difference between N1 and MMN source loci when estimated by using equivalent current dipole fits. Further, our electroencephalography data show a robust MMN after a single standard event when the interval between two consecutive novel sounds is kept invariant. Our converging findings suggest that transient adaptation of feature-specific neurons within human posterior auditory cortex filters superfluous sounds from entering one's awareness.

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