Dissociable mechanisms supporting awareness: the P300 and gamma in a linguistic attentional blink task

Abstract

As demonstrated by the attentional blink (AB) phenomenon, awareness for attended stimuli is governed by sharp capacity limits. We used a linguistic AB task to investigate the neural mechanisms that underlie failures of awareness, examining both event-related potentials and oscillatory brain activity to correctly reported and missed second targets (T2s) presented after a correctly reported first target (T1) in a rapid visual stream of distractors. Correctly reported targets occurring at a short lag (250 ms) after T1-within the classic AB period-elicited enhanced late gamma activity relative to incorrectly reported targets but showed no P300 modulation relative to missed targets. In contrast, correctly reported targets presented at a long lag (830 ms)-outside the classic AB period-elicited a greater P300 component but did not significantly modulate oscillatory activity. This double dissociation suggests that there are multiple neural mechanisms supporting awareness that may operate in parallel. Either the P300 or the gamma can index impairment in the cascade of processing leading to a target's entry into awareness. We conclude that the P300 and gamma activity reflect functionally distinct neural mechanisms, each of which plays an independent role in awareness.

Figure 1.

An example trial. A prime word appeared for 1000 ms, followed by a blank interval for 1000 ms. An RSVP stream (83 ms per frame) was then presented. The first target (T1), consisting of a randomly selected number (between 2 and 9) written out in letters and flanked by Xs to create a 7-character string, occurred randomly between positions 5 through 8. The second target (T2) was a word occurring either 3 positions (250 ms) or ten positions (833 ms) following T1 (i.e., Lag 3 or Lag 10). Distractors were composed of 7-character strings consonants. Distractor items were blue, and T1 and T2 were red. A 1000 ms blank interval followed the RSVP stream, which was then followed by the response period.

Figure 2.

Mean discrimination accuracy for the second target (T2) as a function of lag. For the long lag, T2 appeared 10 frames (833 ms) after T1. For the short lag, T2 appeared 3 frames (250 ms) from T1. Participants reported whether T1 was odd or even, and whether T2 was semantically related or syntactically congruent with the prime (for details, see Batterink et al. 2010). Responses occurred after the end of the trial. Only responses following a correctly reported T1 are included. The decreased accuracy for the short lag demonstrates a significant AB effect. Error bars represent standard error.

Figure 3.

(A). Grand-average ERP waveforms at electrodes Fz, P3, and P4 to second targets (T2s) presented at the short lag (upper panel) and at the long lag (bottom panel), divided as a function of whether they were correctly (green lines) or incorrectly (red lines) reported at the end of the trial. Only trials where T1 was correctly reported are included. The onset of T1 and T2 and the ERPs they elicit, namely visual evoked potentials (VEP, comprising the P1, N1, and P2 components) and P300, are labeled for both the short and the long lag. The P300 was not modulated by awareness at the short lag (n.s.—not significant) but showed a robust effect of awareness at the long lag (*—significant modulation), with correctly reported targets eliciting a greater P300 than missed targets. Insets (right panels) show the topographical distribution of the ERP from 400 to 600 ms, to correctly reported and missed targets at both the short (upper) and the long lag (lower). ERPs were low-pass filtered at 40 Hz for presentation purposes. (B). Topographical voltage maps of difference between correct and incorrect ERPs across latencies corresponding to VEP and P300 effects, at each lag. This awareness effect was computed by subtracting the incorrect ERP from the correct ERP. At the short lag, no ERP effects of awareness were found at any latency. At the long lag, the P300 was significantly enhanced beginning at 200 ms.

Figure 4.

ERSPs measured in dB relative to the prestimulus period [10log₁₀(power₁/power₀)] show oscillatory responses across all scalp electrodes to correctly identified and missed targets at short lags (left panels) and long lags (right panels). Only trials with correctly reported T1s are included. (A) The upper panels show ERSPs following correctly reported second targets (T2s) and the lower panels show ERSPs following incorrectly reported T2s. For a quantitative assessment of overall variability, contour lines indicate the P values of the uncorrected two-tailed t-tests comparing power at each time and frequency bin to prestimulus baseline levels (lines step from P = 0.05 to P = 0.005 to P = 0.0005). The scalp topography of the late gamma response, averaged from 55 to 70 Hz and from 400 to 650 ms, is illustrated for each individual condition. (B) The comparisons of interest were the “awareness effects,” computed by subtracting the missed target ERSP from the correct target ERSP, and are displayed in the bottom panels. These 2 comparisons were subjected to permutation-based cluster thresholding. The late gamma cluster in the short lag awareness ERSP, ranging from approximately 400–650 ms, was the only effect of awareness to survive cluster thresholding and is outlined in magenta with an asterisk. This cluster is indicative of a significant gamma enhancement to correct trials relative to incorrect trials; the scalp topography of this effect, averaged from 55 to 70 Hz and from 400 to 650 ms, is pictured at left. Contour lines represent uncorrected two-tailed P values, stepping from 0.05 to 0.02 to 0.01. Colors indicate power increase (red) or decrease (blue) relative to the 200 ms prestimulus baseline.