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Towards a cognitive neuroscience of self-awareness
•A recurrent dopamine-GABA regulated gamma network is instrumental in self-awareness.•Its anterior and posterior hubs are “ignited” simultaneously with a latency of 160ms.•Gamma oscillations are produced in the hubs by highly oxygen-requiring interneurons.•This makes the hubs vulnerable in penuria,...
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Published in: | Neuroscience and biobehavioral reviews 2017-12, Vol.83, p.765-773 |
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Main Authors: | , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | •A recurrent dopamine-GABA regulated gamma network is instrumental in self-awareness.•Its anterior and posterior hubs are “ignited” simultaneously with a latency of 160ms.•Gamma oscillations are produced in the hubs by highly oxygen-requiring interneurons.•This makes the hubs vulnerable in penuria, resulting in deficient self-monitoring.•Therefore such disorders may be treated unconventionally by targeting interneurons.
Self-awareness is a pivotal component of conscious experience. It is correlated with a paralimbic network of medial prefrontal/anterior cingulate and medial parietal/posterior cingulate cortical “hubs” and associated regions.
Electromagnetic and transmitter manipulation have demonstrated that the network is not an epiphenomenon but instrumental in generation of self-awareness. Thus, transcranial magnetic stimulation (TMS) targeting the hubs impedes different aspects of self-awareness with a latency of 160ms. The network is linked by ∼40Hz oscillations and regulated by dopamine.
The oscillations are generated by rhythmic GABA-ergic inhibitory activity in interneurons with an extraordinarily high metabolic rate. The hubs are richly endowed with interneurons and therefore highly vulnerable to disturbed energy supply. Consequently, deficient paralimbic activity and self-awareness are characteristic features of many disorders with impaired oxygen homeostasis. Such disorders may therefore be treated unconventionally by targeting interneuron function. |
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ISSN: | 0149-7634 1873-7528 |
DOI: | 10.1016/j.neubiorev.2016.04.004 |