Abstract

AIMS Neuroscience Commentary on a special issue on : How do Gamma Frequency Oscillations and NMDA Receptors Contribute to Normal and Dysfunctional Cognitive Performance (Editor: Suresh D Muthukumaraswamy). N-methyl D-aspartate type glutamate receptor antagonists induce schizophreniform disorder symptoms accompanied with deficits in sensory-perception and cognition and with a dramatic and persistent amplification of electroencephalographic baseline gamma frequency (30-80 Hz) oscillations in cortical and subcortical regions, including the thalamus. This generalized network gamma noise might be the source of abnormal activities (e.g, during hallucinations) and disturb function-related synchronized oscillations. The corresponding gamma signal-to-noise ratio is proposed as a potential electrophysiological biomarker of network dysfunctions responsible for disturbances in sensorimotor and cognitive information processing associated with various mental disorders and brain illnesses. Testing theoretical and pathophysiological hypotheses is an appealing and effective basic-clinical translational way to understand how, in health and disease, our brain at work combines its various and miscellaneous molecular, synaptic, cellular and architectural complexities.

Highlights

  • In 1924, Hans Berger invented the cortical electroencephalogram (EEG)

  • Spontaneously-occurring, synchronized and non-synchronized gamma frequency (30–80 Hz) oscillations (GFO) are dominant in the desynchronized cortical EEG [6], a EEG state that can be recorded during conscious awareness in the awake state, executive functions, selective attention [7,8,9], Rapid Eye Movement sleep [10,11], hallucinations [12,13,14,15,16], in early psychosis [17,18], and in the process of meditation [19]

  • N-methyl D-aspartate type glutamate receptors (NMDAr) antagonists transiently disrupt the expression, not the induction, of long-term potentiation in the thalamocortical system (Figure 1B, bottom panel; [63]), disorganize action potential firing in rat prefrontal cortex [64], increase the firing in fast spiking neurons and decrease that in regular spiking neurons [65].These results suggest that the amount of ongoing GFO is inversely related to synaptic potentiation at least in the thalamocortical system [63]

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Summary

AIMS Neuroscience

Received date 9 September 2014, Accepted date 16 September 2014, Published date 19 September 2014.

Introduction
Baseline and Function-Related Network Gamma Oscillations
From Vertical to Horizontal Network Gamma Oscillations
The Dimensional Systems Model and Memory
Ketamine Amplifies Baseline Network Gamma Oscillations
Damped and Forced Harmonic Oscillators
NMDAr-Related Network Dysfunction Modulates the Gamma Signal-To-Noise Ratio
Findings
Conclusion
Full Text
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