Subcortical centers can control consciousness by modulating the readiness of the thalamocortical system without contributing directly to it
It has been known for a long time that lesions in the reticular formation of the brainstem can produce unconsciousness and coma. Conversely, stimulating the reticular formation can arouse a comatose animal and activate the thalamocortical system, making it ready to respond to stimuli . Groups of neurons within the reticular formation are characterized by diffuse projections to many areas of the brain. Many such groups release neuromodulators such as acetylcholine, histamine, noradrenaline, serotonin, dopamine, and glutamate (acting on metabotropic receptors) and can have extremely widespread effects on both neural excitability and plasticity . However, it would seem that the reticular formation, while necessary for the normal functioning of the thalamocortical system and therefore for the occurrence of conscious experience, may not contribute much in terms of specific dimensions of consciousness – it may work mostly like an external on-switch or as a transient booster of thalamocortical firing.
Such a role can be explained readily in terms of information integration. As shown in Fig. 4b, neural elements that have widespread and effective connections to a main complex of high Φ may nevertheless remain informationally excluded from it. Instead, they are part of a larger complex having a much lower value of Φ.
Neural activity in sensory afferents to the thalamocortical system can determine what we experience without contributing directly to it
What we see usually depends on the activity patterns that occur in the retina and that are relayed to the brain. However, many observations suggest that retinal activity does not contribute directly to conscious experience. Retinal cells surely can tell light from dark and convey that information to visual cortex, but their rapidly shifting firing patterns do not correspond well with what we perceive. For example, during blinks and eye movements retinal activity changes dramatically, but visual perception does not. The retina has a blind spot at the exit of the optic nerve where there are no photoreceptors, and it has low spatial resolution and no color sensitivity at the periphery of the visual field, but we are not aware of any of this. More importantly, lesioning the retina does not prevent conscious visual experiences. For example, a person who becomes retinally blind as an adult continues to have vivid visual images and dreams. Conversely, stimulating the retina during sleep by keeping the eyes open and presenting various visual inputs does not yield any visual experience and does not affect visual dreams. Why is it that retinal activity usually determines what we see through its action on thalamocortical circuits, but does not contribute directly to conscious experience?
As shown in Fig. 4c, adding or removing multiple, segregated incoming pathways does not change the composition of the main complex, and causes little change in its Φ. While the incoming pathways do participate in a larger complex together with the elements of the main complex, the Φ value of this larger complex is very low, being limited by the effective information between each afferent pathway and its port in at the main complex. Thus, input pathways providing powerful inputs to a complex add nothing to the information it integrates if their effects are entirely accounted for by ports-in.
Neural activity in motor efferents from the thalamocortical system, while producing varied behavioral outputs, does not contribute directly to conscious experience
In neurological practice, as well as in everyday life, we tend to associate consciousness with the presence of a diverse behavioral repertoire. For example, if we ask a lot of different questions and for each of them we obtain an appropriate answer, we generally infer that a person is conscious. Such a criterion is not unreasonable in terms of information integration, given that a wide behavioral repertoire is usually indicative of a large repertoire of internal states that are available to an integrated system. However, it appears that neural activity in motor pathways, which is necessary to bring about such diverse behavioral responses, does not in itself contribute to consciousness. For example, patients with the locked-in syndrome, who are completely paralyzed except for the ability to gaze upwards, are fully conscious. Similarly, while we are completely paralyzed during dreams, consciousness is not impaired by the absence of behavior. Even lesions of central motor areas do not impair consciousness.
Why is it that neurons in motor pathways, which can produce a large repertoire of different outputs and thereby relay a large amount of information about different conscious states, do not contribute directly to consciousness? As shown in Fig. 4d, adding or removing multiple, segregated outgoing pathways to a main complex does not change the composition of the main complex, and does not change its Φ value. Like incoming pathways, outgoing pathways do participate in a larger complex together with the elements of the main complex, but the Φ value of this larger complex is very low, being limited by the effective information between each port-out of the main complex and its effector targets.