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  • Pratt._et_2015_FINAL (1)

    Rights statement: This is the author’s version of a work that was accepted for publication in Schizophrenia Research. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Schizophrenia Research, 180, 2017 DOI: 10.1016/j.schres.2016.05.013

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

Research output: Contribution to journalJournal article

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  • Judith Pratt
  • Neil Dawson
  • Brian J. Morris
  • Tineke Grent-'t-Jong
  • Frederic Roux
  • Peter J. Uhlhaas
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<mark>Journal publication date</mark>02/2017
<mark>Journal</mark>Schizophrenia Research
Volume180
Number of pages9
Pages (from-to)4-12
Publication statusPublished
Early online date14/06/16
Original languageEnglish

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.

Bibliographic note

This is the author’s version of a work that was accepted for publication in Schizophrenia Research. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Schizophrenia Research, 180, 2017 DOI: 10.1016/j.schres.2016.05.013