Searching for the mismatch negativity in primary auditory cortex of the awake monkey: Deviance detection or stimulus specific adaptation?

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Abstract

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 populationortoafrequency that evokedaresponse half the amplitudeof 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 stan-dardsofthe 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 macaqueA1reflect stimulus-specific adaptation rather than deviance detection per se.We conclude that neural mechanismsofdeviance detection likely reside in cortical areas outside of A1.

Original languageEnglish (US)
Pages (from-to)15747-15758
Number of pages12
JournalJournal of Neuroscience
Volume32
Issue number45
DOIs
StatePublished - Nov 7 2012

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Auditory Cortex
Haplorhini
Macaca
Evoked Potentials
Acoustics
Brain

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

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title = "Searching for the mismatch negativity in primary auditory cortex of the awake monkey: Deviance detection or stimulus specific adaptation?",
abstract = "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 populationortoafrequency that evokedaresponse half the amplitudeof 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 stan-dardsofthe 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 macaqueA1reflect stimulus-specific adaptation rather than deviance detection per se.We conclude that neural mechanismsofdeviance detection likely reside in cortical areas outside of A1.",
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