Abstract
Mismatch negativity (MMN) is a component of event-related potentials (ERPs) evoked by violations of regularity in sensory stimulus-series in humans. Recently, the MMN has received attention as a clinical and translatable biomarker of psychiatric disorders such as schizophrenia, and for the development animal models of these psychiatric disorders. In this study, we investigated the generation of MMN in common marmosets, which are an important non-human primate model with genetic manipulability. We recorded the electrocorticograms (ECoGs) from two common marmosets with epidurally implanted electrodes covering a wide range of cortical regions. ECoG recordings were conducted in a passive listening condition with a roving oddball paradigm. We compared the ERPs evoked by repeatedly presented standard stimuli and those evoked by the deviant stimuli. Significant differences in the ERPs were observed in several cortical areas. In particular, deviant stimuli elicited larger negative activity than standard stimuli in the temporal area. In addition, the latency and polarity of the activity were comparable to human MMNs. This is thus the first report of MMN-like activity in common marmosets. Our findings have the potential to advance future gene-manipulation studies that aim to establish non-human primate models of schizophrenia.
Highlights
Mismatch negativity (MMN) is a component of event-related potentials (ERPs) evoked by violations of regularity in sensory stimulus-series in humans
Et al.[4] reported that “at-risk mental state” (ARMS) subjects who later developed schizophrenia elicited smaller MMN amplitudes compared to those of healthy controls, while no such difference was found for ARMS subjects who did not transition to schizophrenia
We investigated the generation of MMN in common marmosets
Summary
Mismatch negativity (MMN) is a component of event-related potentials (ERPs) evoked by violations of regularity in sensory stimulus-series in humans. We investigated the generation of MMN in common marmosets, which are an important non-human primate model with genetic manipulability. Et al.[4] reported that “at-risk mental state” (ARMS) subjects who later developed schizophrenia elicited smaller MMN amplitudes compared to those of healthy controls, while no such difference was found for ARMS subjects who did not transition to schizophrenia. These results suggest that MMN could be used as a physiological biomarker for the early diagnosis of schizophrenia. We hypothesised that common marmosets would be sensitive to this paradigm
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
