A hypothetical neural mechanism for inattentional blindness
DOI:
https://doi.org/10.33910/2687-1270-2022-3-1-23-40Keywords:
voluntary attention, synaptic plasticity, dopamine, neocortex, thalamus, basal ganglia, hippocampus, cerebellumAbstract
One of the approaches to neuroscientific investigation of consciousness is the study of inattentional blindness. Since this effect is the result of the absence of voluntary attention, it is highly interesting to study the latter. We proposed that the involvement of voluntary attention into the processing of sensory information requires the activation of prefrontal cortex and hippocampus, as well as a release of dopamine in the input structure of the basal ganglia, the striatum. This promotes disinhibition of neurons in the thalamus, subthalamic and pedunculopontine nuclei experiencing inhibitory influence of the basal ganglia. If neurons of the ventral striatum (where, the inputs converge from the hippocampus and the prefrontal and retrosplenial cortical areas) are activated strongly enough, the dopamine-dependent activity reorganization in the cortico-basal ganglia-thalamo-cortical loops facilitates the generation of neuronal representations of sensory stimuli in the corresponding neocortical areas. In addition, it creates the conditions for the circulation of excitation in the topographically organized thalamo-cortical loops, the loops connecting primary and higher cortical areas through high order thalamic nuclei, and loops connecting the neocortex and thalamus with the hippocampus, cerebellum, subthalamic and pedunculopontine nuclei. It is generally accepted that conscious perception is facilitated by re-excitation of higher cortical areas. If so, the time required for the conscious perception of a sensory stimulus should depend on the time of activity circulates in the loops mentioned earlier. It follows from the proposed mechanism that dopamine deficiency increases inhibition of the thalamus and decreases its excitation by the neocortex, cerebellum, subthalamic and pedunculopontine nuclei. This should lead to an increase in the interval between the two stimuli required to become aware of the second one. This consequence is in line with the well-known results of studies of inattentional blindness. They showed a similar increase in this interval in Parkinson’s disease and due to the damage of the cerebellum or pedunculopontine nucleus.
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