Journal
JOURNAL OF NEUROSCIENCE
Volume 32, Issue 45, Pages 15747-15758Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.2835-12.2012
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Funding
- NIH [DC00657]
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The mismatch negativity (MMN) is a preattentive component of the auditory event-related potential that is elicited by a change in a repetitive acoustic pattern. While MMN has been extensively used in human electrophysiological studies of auditory processing, the neural mechanisms and brain regions underlying its generation remain unclear. We investigate possible homologs of the MMN in macaque primary auditory cortex (A1) using a frequency oddball paradigm in which rare deviant tones are randomly interspersed among frequent standard tones. Standards and deviants had frequencies equal to the best frequency (BF) of the recorded neural population or to a frequency that evoked a response half the amplitude of the BF response. Early and later field potentials, current source density components, multiunit activity, and induced high-gamma band responses were larger when elicited by deviants than by standards of the same frequency. Laminar analysis indicated that differences between deviant and standard responses were more prominent in later activity, thus suggesting cortical amplification of initial responses driven by thalamocortical inputs. However, unlike the human MMN, larger deviant responses were characterized by the enhancement of obligatory responses rather than the introduction of new components. Furthermore, a control condition wherein deviants were interspersed among many tones of variable frequency replicated the larger responses to deviants under the oddball condition. Results suggest that differential responses under the oddball condition in macaque A1 reflect stimulus-specific adaptation rather than deviance detection per se. We conclude that neural mechanisms of deviance detection likely reside in cortical areas outside of A1.
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