Thalamo-cortical communication, glutamatergic neurotransmission and neural oscillations: a unique window into the origins of ScZ?

Judith Pratt, Neil Dawson, Brain J. Morris, Tineke Grent T'Jong, Frederic Roux, Peter J. Uhlhaas

Research output: Contribution to journalArticle

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Abstract

The thalamus has recently received renewed interest in systems-neuroscience and schizophrenia (ScZ) research because of emerging evidence highlighting its important role in coordinating functional interactions in cortical-subcortical circuits. Moreover, higher cognitive functions, such as working memory and attention, have been related to thalamo-cortical interactions, providing a novel perspective for the understanding of the neural substrate of cognition. The current review will support this perspective by summarizing evidence on the crucial role of neural oscillations in facilitating thalamo-cortical (TC) interactions during normal brain functioning and their potential impairment in ScZ. Specifically, we will focus on the relationship between NMDA-R mediated (glutamatergic) neurotransmission in TC-interactions. To this end, we will first review the functional anatomy and neurotransmitters in thalamic circuits, followed by a review of the oscillatory signatures and cognitive processes supported by TC-circuits. In the second part of the paper, data from preclinical research as well as human studies will be summarized that have implicated TC-interactions as a crucial target for NMDA-receptor hypofunctioning. Finally, we will compare these neural signatures with current evidence from ScZ-research, suggesting a potential overlap between alterations in TC-circuits as the result of NMDA-R deficits and stage-specific alterations in large-scale networks in ScZ.

Original languageEnglish
Pages (from-to)4-12
Number of pages9
JournalSchizophrenia Research
Volume180
Early online date14 Jun 2016
DOIs
Publication statusPublished - Feb 2017
Externally publishedYes

Keywords

  • thalamus
  • schizophrenia
  • neural oscillations
  • NMDA receptor
  • glutamate

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