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Neuroscience and Psychiatry |

Low-Frequency Brain Oscillations in Schizophrenia

John Lisman, PhD1
[+] Author Affiliations
1Department of Biology and Volen Center for Complex Systems, Brandeis University, Waltham, Massachusetts
JAMA Psychiatry. 2016;73(3):298-299. doi:10.1001/jamapsychiatry.2015.2320.
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This review reports on what has been learned about the network mechanisms that underlie abnormal delta oscillations.

Understanding the brain networks that produce the symptoms of schizophrenia is a major goal of modern neuroscience. There is increasing evidence that brain function depends critically on oscillations, and it has therefore been of interest to determine whether the oscillatory properties of the brain are abnormal in schizophrenic patients. There is now considerable evidence that this is the case; indeed, both gamma frequency oscillations (30-80 Hz) and low-frequency oscillations (delta oscillations of 1-4 Hz and theta oscillations of 5-10 Hz) in the electroencephalogram (EEG) show well-replicated abnormalities but with different relationships to the disease state. A reduction in task-evoked gamma power is present in unaffected relatives of schizophrenic patients and may therefore be an endophenotype of the disease, but not a direct cause. In contrast, the increased power of resting delta oscillations is present only when the disease is present and may therefore be directly causal.1,2

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Figure.
Model of How the Elevated Delta Oscillations in Schizophrenia Interfere With Working Memory

The nucleus reuniens, one of several midline thalamic relay nuclei, may interfere with communication from the medial prefrontal cortex (mPFC) to the hippocampus. N-methyl-d-aspartate receptors (NMDARs), D2 receptors, and T channels have been implicated in schizophrenia by genome-wide association studies. A, In a spatial working memory task, experiments in rodents7 show that working memory information in the mPFC is transmitted to the nucleus reuniens and from there to the hippocampus, where it informs the spatial processing necessary for the task. B, Abnormal delta frequency bursting in the nucleus reuniens jams communication of working memory information and may thereby produce working memory deficits. C, Delta oscillations are generated through an interaction of the relay nuclei and the γ-aminobutyric acid–ergic cells of the nucleus reticularis and depend on functional T-type calcium (Ca2+) channels. These channels are inactivated by a depolarization produced by a basal current through NR2C (or by block of D2 receptors). D, Block of NR2C produces hyperpolarization, which deinactivates T channels. These channels then produce delta frequency bursting, which in turn results in delta frequency bursting of the nucleus reuniens.

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