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

Schizophr Res. 2017 Feb:180:4-12. doi: 10.1016/j.schres.2016.05.013. Epub 2016 Jun 14.

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: Glutamate; NMDA-receptors; Neural oscillations; Schizophrenia; Thalamus.

Publication types

  • Review

MeSH terms

  • Animals
  • Brain Waves / physiology
  • Cerebral Cortex / pathology
  • Cerebral Cortex / physiopathology*
  • Glutamic Acid / metabolism*
  • Humans
  • Neural Pathways / pathology
  • Neural Pathways / physiopathology
  • Receptors, N-Methyl-D-Aspartate / metabolism
  • Schizophrenia / pathology
  • Schizophrenia / physiopathology*
  • Synaptic Transmission / physiology*
  • Thalamus / pathology
  • Thalamus / physiopathology*

Substances

  • Receptors, N-Methyl-D-Aspartate
  • Glutamic Acid