Mismatch negativity: translating the potential

Abstract

The mismatch negativity (MMN) component of the auditory event-related potential has become a valuable tool in cognitive neuroscience. Its reduced size in persons with schizophrenia is of unknown origin but theories proposed include links to problems in experience-dependent plasticity reliant on N-methyl-d-aspartate glutamate receptors. In this review we address the utility of this tool in revealing the nature and time course of problems in perceptual inference in this illness together with its potential for use in translational research testing animal models of schizophrenia-related phenotypes. Specifically, we review the reasons for interest in MMN in schizophrenia, issues pertaining to the measurement of MMN, its use as a vulnerability index for the development of schizophrenia, the pharmacological sensitivity of MMN and the progress in developing animal models of MMN. Within this process we highlight the challenges posed by knowledge gaps pertaining to the tool and the pharmacology of the underlying system.

Keywords: NMDA; NMDAR; auditory event-related potential; mismatch negativity; schizophrenia; synaptic plasticity.

Figure 1

Schematic of sequence design showing sequences with deviants presented at a probability of 0.125 (1/8), two oddball sequences are presented in a flip-flop design (A), controlling for the physical characteristics of the stimuli. Differential adaptation can be controlled for through the use of a deviant-alone control (B), which presents the deviant at the same temporal rate as it is presented in the oddball sequence, but without the intervening standards; or the many-standards control (C), which presents several stimuli (including the deviant) at the same temporal rate as the oddball sequences.