The reduced detectability of a target T2 following discrimination of a preceding target T1 in the attentional blink (AB) paradigm is classically interpreted as a consequence of reduced attention to T2 due to attentional allocation to T1. Here, we investigated whether AB was related to changes in microsaccade rate (MSR). We found a pronounced MSR signature following T1 onset, characterized by MSR suppression from 200 to 328 ms and enhancement from 380 to 568 ms. Across participants, the magnitude of the MSR suppression correlated with the AB effect such that low T2 detectability corresponded to reduced MSR. However, in the same task, T1 error trials coincided with the presence of microsaccades. We discuss this apparent paradox in terms of known neurophysiological correlates of MS whereby cortical excitability is suppressed both during the microsaccade and MSR suppression, in accordance to poor T1 performance with microsaccade occurrence and poor T2 performance with microsaccade absence. Our data suggest a novel low-level mechanism contributing to AB characterized by reduced MSR, thought to cause suppressed visual cortex excitability. This opens the question of whether attention mediates T2 performance suppression independently from MSR, and if not, how attention interacts with MSR to produce the T2 performance suppression.

中文翻译：

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注意闪烁与微扫视速率签名有关。

经典地解释了在注意眨眼（AB）范式中对先前目标T1的辨别后目标T2的可检测性降低，这通常被解释为由于对T1的注意力分配而导致对T2的关注减少。在这里，我们调查了AB是否与微扫视率（MSR）的变化有关。我们在T1发作后发现了明显的MSR签名，其特征是MSR抑制从200到328毫秒，增强从380到568毫秒。在所有参与者中，MSR抑制的幅度与AB效应相关，因此较低的T2可检测性对应于降低的MSR。但是，在同一任务中，T1错误试验与微扫视同时出现。我们根据已知的MS的神经生理相关性讨论这种明显的悖论，据此，在微扫视和MSR抑制过程中，皮层兴奋性均受到抑制，这与微扫视发生时的T1性能差和无微扫视时的T2性能差有关。我们的数据表明，一种新型的低级机制有助于AB，其特征是MSR降低，认为导致视皮层兴奋性降低。这就提出了一个问题，即注意力是否独立于MSR介导T2性能抑制，如果不是，则注意力如何与MSR相互作用以产生T2性能抑制。我们的数据表明，一种新型的低级机制有助于AB，其特征是MSR降低，认为导致视皮层兴奋性降低。这就提出了一个问题，即注意力是否独立于MSR介导T2性能抑制，如果不是，则注意力如何与MSR相互作用以产生T2性能抑制。我们的数据表明，一种新型的低级机制有助于AB，其特征是MSR降低，认为导致视皮层兴奋性降低。这就提出了一个问题，即注意力是否独立于MSR介导T2性能抑制，如果不是，则注意力如何与MSR相互作用以产生T2性能抑制。