Abstract

This study proposes a computational model for attentional blink or “blink of the mind,” a phenomenon where a human subject misses perception of a later expected visual pattern as two expected visual patterns are presented less than 500 ms apart. A neocortical patch modeled as an attractor network is stimulated with a sequence of 14 patterns 100 ms apart, two of which are expected targets. Patterns that become active attractors are considered recognized. A neocortical patch is represented as a square matrix of hypercolumns, each containing a set of minicolumns with synaptic connections within and across both minicolumns and hypercolumns. Each minicolumn consists of locally connected layer 2/3 pyramidal cells with interacting basket cells and layer 4 pyramidal cells for input stimulation. All neurons are implemented using the Hodgkin–Huxley multi-compartmental cell formalism and include calcium dynamics, and they interact via saturating and depressing AMPA/NMDA and GABAA synapses. Stored patterns are encoded with global connectivity of minicolumns across hypercolumns and active patterns compete as the result of lateral inhibition in the network. Stored patterns were stimulated over time intervals to create attractor interference measurable with synthetic spike traces. This setup corresponds with item presentations in human visual attentional blink studies. Stored target patterns were depolarized while distractor patterns where hyperpolarized to represent expectation of items in working memory. Simulations replicated the basic attentional blink phenomena and showed a reduced blink when targets were more salient. Studies on the inhibitory effect of benzodiazepines on attentional blink in human subjects were compared with neocortical simulations where the GABAA receptor conductance and decay time were increased. Simulations showed increases in the attentional blink duration, agreeing with observations in human studies. In addition, sensitivity analysis was performed on key parameters of the model, including Ca2+-gated K+ channel conductance, synaptic depression, GABAA channel conductance and the NMDA/AMPA ratio of charge entry.

Highlights

  • The phenomenon of attentional blink (AB) was first observed by Broadbent and Broadbent (1987) and later reported as an attentional limit by Raymond et al (1992)

  • The percentage of active attractors is hypothesized to be equivalent to the percentage of correctly reported items during an AB rapid serial visual presentation (RSVP) experiment

  • The simulation results reproduce the basic AB but do not produce lag 1 sparing, as can happen when items in the RSVP stream are spatially shifted (Visser et al, 1999b) or due to attentional switching (Visser et al, 1999a). This suggests that the lag 1 sparing phenomenon represents a separate mechanism to the AB effect, which is not represented by our model

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Summary

Introduction

The phenomenon of attentional blink (AB) was first observed by Broadbent and Broadbent (1987) and later reported as an attentional limit by Raymond et al (1992). It occurs when two expected stimulus items are presented less than 500 ms apart. In the dual-task experiment, the subject is told to report on two targets T1 followed by T2 presented serially each trial, if they occur. If T2 is presented before an attended T1 has finished processing the second stage, recognition of T2 can be lost and will not reach working memory. The theory asserts that AB results from a refractory period of NE release which lasts about 500 ms

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