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“Cortical Mapping Of Mismatch Negativity With Deviance Detection Property In Rat.” Metadata:

  • Title: ➤  Cortical Mapping Of Mismatch Negativity With Deviance Detection Property In Rat.
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  • Language: English

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  • Internet Archive ID: pubmed-PMC3861386

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This article is from <a href="//archive.org/search.php?query=journaltitle%3A%28PLoS%20ONE%29" rel="ugc nofollow">PLoS ONE</a>, <a href="//archive.org/search.php?query=journaltitle%3A%28PLoS%20ONE%29%20AND%20volume%3A%288%29" rel="ugc nofollow">volume 8</a>.<h2>Abstract</h2>Mismatch Negativity (MMN) is an N-methyl-d-aspartic acid (NMDA)-mediated, negative deflection in human auditory evoked potentials in response to a cognitively discriminable change. MMN-like responses have been extensively investigated in animal models, but the existence of MMN equivalent is still controversial. In this study, we aimed to investigate how closely the putative MMN (MMNp) in rats exhibited the comparable properties of human MMN. We used a surface microelectrode array with a grid of 10×7 recording sites within an area of 4.5×3.0 mm to densely map evoked potentials in the auditory cortex of anesthetized rats under the oddball paradigm. Firstly, like human MMN, deviant stimuli elicited negative deflections in auditory evoked potentials following the positive middle-latency response, termed P1. Secondly, MMNp exhibited deviance-detecting property, which could not be explained by simple stimulus specific adaptation (SSA). Thirdly, this MMNp occurred focally in the auditory cortex, including both the core and belt regions, while P1 activation focus was obtained in the core region, indicating that both P1 and MMNp are generated in the auditory cortex, yet the sources of these signals do not completely overlap. Fourthly, MMNp significantly decreased after the application of AP5 (D-(-)-2-amino-5-phosphonopentanoic acid), an antagonist at NMDA receptors. In stark contrast, AP5 affected neither P1 amplitude nor SSA of P1. These results provide compelling evidence that the MMNp we have examined in rats is functionally comparable to human MMN. The present work will stimulate translational research into MMN, which may help bridge the gap between electroencephalography (EEG)/magnetoencephalography (MEG) studies in humans and electrophysiological studies in animals.

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