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.

Evidence for modality-specific but not frequency-specific modulation of human primary auditory cortex by attention.

We used the stimulus-driven 40-Hz auditory steady-state response (ASSR) that localizes tonotopically to the region of primary auditory cortex (A1) to study modulation of this region by top-down attention. Experiment 1 presented amplitude modulated (AM) auditory and visual stimuli simultaneously (AM at 40 Hz and 16 Hz, respectively) while participants responded to targets in one modality or the other. ASSR amplitude increased from an unattended passive baseline during auditory but not visual attention demonstrating modality-specific auditory attention, when attention was required for brief (1 s) but not long (2 min) time intervals. Modality-specific visual attention occurred at both time intervals. Experiment 2 asked whether attention directed to one or the other of two simultaneous auditory streams (carrier frequencies of 250 and 4100 Hz AM at 37 and 41 Hz respectively, counterbalanced) increased ASSR amplitude for the attended stream (frequency-specific auditory attention). Behaviour was strongly controlled by carrier frequency (overall target rate 1.7 Hz), and the cortical sources of the two carriers were resolved by inverse modeling. Despite these conditions favourable to frequency specificity, frequency-specific modulation of ASSR amplitude was not found at either time interval. Frequency-specific modulation of A1 may require re-entrant feedback to the auditory core from auditory percepts that possess distinct spectral attributes and are attended in higher regions of the auditory system.

Evidence for fusion and segregation induced by 21 Hz multiple-digit stimulation in humans.

Subjects were trained to detect changes in the frequency of 21 Hz tactile stimulation applied to digits 2 + 3 + 4 (fusion group) or 2 + 4 (segregation group) of the right hand. The 21 Hz steady-state response for digit 3 was measured by 64 channel EEG on mapping trials before and after training. Discrimination improved over 3 days, confirming that subjects attended to the training stimuli. The 21 Hz response was larger on training than on mapping trials, indicating sensitivity of the response to the strength of cortical activation. Under these conditions the 21 Hz response for digit 3 decreased after training in both groups on day 1. On day 3 this effect reversed in a subset of fusion subjects while segregation continued to yield decreases. The findings suggest that somatosensory representations are dynamically modified by the sensory input experienced on a task.