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

  title={Thalamo-cortical communication, glutamatergic neurotransmission and neural oscillations: A unique window into the origins of ScZ?},
  author={Judith A. Pratt and Neil Dawson and Brain J. Morris and Tineke Grent-'t-Jong and Frederic Roux and Peter J. Uhlhaas},
  journal={Schizophrenia Research},
Visual Attention Deficits in Schizophrenia Can Arise From Inhibitory Dysfunction in Thalamus or Cortex
A spiking neural network model is developed that demonstrates how dysfunctional inhibition can degrade attentive gaze control and support the search for new eye movement metrics that may index distinct underlying neural defects in schizophrenia.
A MEG Study of Visual Repetition Priming in Schizophrenia: Evidence for Impaired High-Frequency Oscillations and Event-Related Fields in Thalamo-Occipital Cortices
Although behavioral priming was preserved, patients with schizophrenia showed deficits in repetition suppression as well as repetition enhancement in thalamic and occipital regions, suggesting that experience-dependent modification of neural circuits is impaired in the disorder.
Disruption of gamma–delta relationship related to working memory deficits in first-episode psychosis
An inability to encode multiple items in short-term memory associated with abnormalities in the relationship between oscillations related to the difficulty of the WM task is demonstrated in FEP, arguing in favor of a dysfunction of the E/I balance in psychosis.
Acute ketamine dysregulates task-related gamma-band oscillations in thalamo-cortical circuits in schizophrenia
It is shown that treating healthy controls with ketamine triggers changes in neural oscillations during visual processing distinct from those seen in patients with schizophrenia, suggesting that acute NMDA receptor hypofunction does not account for visuo-perceptual deficits in the disorder.
Deconstructing Schizophrenia: Advances in Preclinical Models for Biomarker Identification.
This review will highlight recent research of preclinical biomarkers in schizophrenia that show the most promise for informing clinical needs with an emphasis on relevant imaging, electrophysiological, cognitive behavioural and biochemical modalities.


The thalamic reticular nucleus: A functional hub for thalamocortical network dysfunction in schizophrenia and a target for drug discovery
The thalamic reticular nucleus (TRN) is focused on providing evidence for it being an important communication hub between the thalamus and cortex and how it may play a key role in the pathophysiology of schizophrenia.
Dysfunctional thalamus-related networks in schizophrenia.
  • D. Pinault
  • Psychology, Biology
    Schizophrenia bulletin
  • 2011
The thalamic reticular nucleus is a thin GABAergic layer interface strategically located between the thalamus and the neocortex that forms 2-neuron open-loop circuits that contribute to a lack of coordination in activity between brain regions, as observed in psychiatric disorders like schizophrenia.
A new mode of corticothalamic transmission revealed in the Gria4−/− model of absence epilepsy
A previously unknown mode of cortico-thalamo-cortical transmission is revealed, bypassing direct cortICO-nRT excitation, and a mechanism for pathological oscillation generation is described.
Thalamocortical dysconnectivity in schizophrenia.
The etiology of schizophrenia may disrupt the development of prefrontal-thalamic connectivity and refinement of somatomotor connectivity with the thalamus that occurs during brain maturation, establishing differential abnormalities of thalamocortical networks in schizophrenia.
Ketamine-Induced Modulation of the Thalamo-Cortical Network in Healthy Volunteers As a Model for Schizophrenia
The results indicate that changes of thalamic functioning as described for schizophrenia can be partly mimicked by NMDA-receptor blockage, which adds substantial knowledge about the neurobiological mechanisms underlying the profound changes of perception and behavior during the application of NMDA -receptor antagonists.
Inhibition of Mediodorsal Thalamus Disrupts Thalamofrontal Connectivity and Cognition
Sustained NMDA receptor hypofunction induces compromised neural systems integration and schizophrenia-like alterations in functional brain networks.
It is proposed that sustained NMDA receptor hypofunction contributes to the pathophysiology of dysfunctional brain network organization in schizophrenia.
The thalamic reticular nucleus and schizophrenia.
It is suggested that this thalamic GABAergic nucleus may be involved in the neurobiology of schizophrenia, and deficits in attention and sensory gating have been consistently found in schizophrenics, including first-break and chronic patients.
Dysconnection in Schizophrenia: From Abnormal Synaptic Plasticity to Failures of Self-monitoring
It is argued that this neurobiological mechanism can explain failures of self-monitoring, leading to a mechanistic explanation for first-rank symptoms as pathognomonic features of schizophrenia, and may provide a basis for future diagnostic classifications with physiologically defined patient subgroups.