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Mechanisms of adaptation in human auditory cortex
Author(s) -
Cris Lanting,
Paul M. Briley,
Christian J. Sumner,
Katrin Krumbholz
Publication year - 2013
Publication title -
journal of neurophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.302
H-Index - 245
eISSN - 1522-1598
pISSN - 0022-3077
DOI - 10.1152/jn.00547.2012
Subject(s) - neuroscience , auditory cortex , adaptation (eye) , psychology , communication , cortex (anatomy) , cognitive psychology
This study investigates the temporal properties of adaptation in the late auditory-evoked potentials in humans. The results are used to make inferences about the mechanisms of adaptation in human auditory cortex. The first experiment measured adaptation by single adapters as a combined function of the adapter duration and the stimulus onset asynchrony (SOA) and interstimulus interval (ISI) between the adapter and the adapted sound ("probe"). The results showed recovery from adaptation with increasing ISI, as would be expected, but buildup of adaptation with increasing adapter duration and thus SOA. This suggests that adaptation in auditory cortex is caused by the ongoing, rather than the onset, response to the adapter. Quantitative modeling indicated that the rate of buildup of adaptation is almost an order of magnitude faster than the recovery rate of adaptation. The recovery rate suggests that cortical adaptation is caused by synaptic depression and slow afterhyperpolarization. The P2 was more strongly affected by adaptation than the N1, suggesting that the two deflections originate from different cortical generators. In the second experiment, the single adapters were replaced by trains of two or four identical adapters. The results indicated that adaptation decays faster after repeated presentation of the adapter. This increase in the recovery rate of adaptation might contribute to the elicitation of the auditory mismatch negativity response. It may be caused by top-down feedback or by local processes such as the buildup of residual Ca(2+) within presynaptic neurons.

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