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    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?

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Thalamo-cortical communication, glutamatergic neurotransmission and neural oscillations: a unique window into the origins of ScZ? / Pratt, Judith; Dawson, Neil; Morris, Brian J. et al.
In: Schizophrenia Research, Vol. 180, 02.2017, p. 4-12.

Research output: Contribution to Journal/MagazineJournal articlepeer-review

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Pratt J, Dawson N, Morris BJ, Grent-'t-Jong T, Roux F, Uhlhaas PJ. Thalamo-cortical communication, glutamatergic neurotransmission and neural oscillations: a unique window into the origins of ScZ? Schizophrenia Research. 2017 Feb;180:4-12. Epub 2016 Jun 14. doi: 10.1016/j.schres.2016.05.013

Author

Pratt, Judith ; Dawson, Neil ; Morris, Brian J. et al. / Thalamo-cortical communication, glutamatergic neurotransmission and neural oscillations : a unique window into the origins of ScZ?. In: Schizophrenia Research. 2017 ; Vol. 180. pp. 4-12.

Bibtex

@article{a2d7f8bdd899422d9235a06de3059420,
title = "Thalamo-cortical communication, glutamatergic neurotransmission and neural oscillations: a unique window into the origins of ScZ?",
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.",
keywords = "Thalamus, Schizophrenia, Neural oscillations, NMDA-receptors, Glutamate",
author = "Judith Pratt and Neil Dawson and Morris, {Brian J.} and Tineke Grent-'t-Jong and Frederic Roux and Uhlhaas, {Peter J.}",
note = "This is the author{\textquoteright}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",
year = "2017",
month = feb,
doi = "10.1016/j.schres.2016.05.013",
language = "English",
volume = "180",
pages = "4--12",
journal = "Schizophrenia Research",
issn = "0920-9964",
publisher = "ELSEVIER SCIENCE BV",

}

RIS

TY - JOUR

T1 - Thalamo-cortical communication, glutamatergic neurotransmission and neural oscillations

T2 - a unique window into the origins of ScZ?

AU - Pratt, Judith

AU - Dawson, Neil

AU - Morris, Brian J.

AU - Grent-'t-Jong, Tineke

AU - Roux, Frederic

AU - Uhlhaas, Peter J.

N1 - 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

PY - 2017/2

Y1 - 2017/2

N2 - 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.

AB - 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.

KW - Thalamus

KW - Schizophrenia

KW - Neural oscillations

KW - NMDA-receptors

KW - Glutamate

U2 - 10.1016/j.schres.2016.05.013

DO - 10.1016/j.schres.2016.05.013

M3 - Journal article

VL - 180

SP - 4

EP - 12

JO - Schizophrenia Research

JF - Schizophrenia Research

SN - 0920-9964

ER -