Acoustic experience but not attention modifies neural population phase expressed in human primary auditory cortex

We studied the effect of auditory training on the 40-Hz auditory steady-state response (ASSR) known to localize tonotopically to the region of primary auditory cortex (A1). The stimulus procedure was designed to minimize competitive interactions among frequency representations in A1 and delivered target events at random times in a training window, to increase the likelihood that neuroplastic changes could be detected. Experiment 1 found that repeated exposure to this stimulus advanced the phase of the ASSR (shortened the time delay between the 40-Hz response and stimulus waveforms). The phase advance appeared at the outset of the second of two sessions separated by 24–72 h, did not require active training, and was not accompanied by changes in ASSR amplitude over this time interval. Experiment 2 applied training for 10 sessions to reveal further advances in ASSR phase and also an increase in ASSR amplitude, but the amplitude effect lagged that on phase and did not correlate with perceptual performance while the phase advance did. A control group trained for a single session showed a phase advance but no amplitude enhancement when tested 6 weeks later (retention). In both experiments attention to auditory signals increased ASSR amplitude but had no effect on ASSR phase. Our results reveal a persistent form of neural plasticity expressed in the phase of ASSRs generated from the region of A1, which occurs either in A1 or in subcortical nuclei projecting to this region.

Research highlights
► Auditory training advanced the phase of the 40-Hz auditory steady state response (ASSR).
► This plastic effect was expressed in human primary auditory cortex.
► Phase also advanced when sounds were presented in the background without training.
► ASSR amplitude was increased by attention but ASSR phase was not.
► ASSR amplitude and phase reflect dissociable underlying mechanisms.