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Ketamine has been found to increase brain noise

Ketamine has been found to increase brain noise

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Summary: By inhibiting NMDA receptors, ketamine increases noise to gamma frequencies in one layer of the thalamic nucleus and one layer of the somatosensory cortex. The findings suggest that psychosis may be triggered by an increase in background noise damaging thalamocortical neurons, which may be caused by a malfunction in NMDA receptors affecting the balance of inhibition and excitation in the brain.

source: HSE

An international team of researchers, including Sofia Kulikova, senior research fellow at HSE University-Perm, found that ketamine, as an NMDA receptor inhibitor, increases the brain’s background noise, causing a higher entropy of incoming sensory signals and disrupting their transmission between the thalamus and the bark.

This finding may contribute to a better understanding of the causes of psychosis in schizophrenia.

An article with the results of the study was published in European Journal of Neuroscience.

Schizophrenia spectrum disorders affect approximately one in 300 people worldwide. The most common manifestations of these disorders are perceptual disturbances such as hallucinations, delusions, and psychoses.

A drug called ketamine can cause a mental state similar to psychosis in healthy individuals. Ketamine inhibits NMDA receptors involved in the transmission of excitatory signals in the brain. An imbalance of excitation and inhibition in the central nervous system can affect the accuracy of sensory perception.

Such changes in the functioning of NMDA receptors are now believed to be one of the causes of perceptual disturbances in schizophrenia. However, it is not yet clear how exactly this process occurs in the affected areas of the brain.

To find out, neuroscientists from France, Austria, and Russia studied how the brains of ketamine-addicted lab rats process sensory signals. The researchers studied beta and gamma oscillations that occur in response to sensory stimuli in the thalamocortical system of the rodent brain, a neural network connecting the cerebral cortex to the thalamus responsible for transmitting sensory information from the perceptual organs to the brain.

Beta oscillations are brain waves in the range of 15 to 30 Hz, and gamma waves are those in the range of 30 to 80 Hz. These frequencies are thought to be critical for encoding and integrating sensory information.

In the rat experiment, microelectrodes were implanted to record electrical activity in the thalamus and somatosensory cortex, a region of the brain responsible for processing sensory information coming from the thalamus. The researchers stimulated the rats’ whiskers (vibrissae) and recorded brain responses before and after administration of ketamine.

Comparison of the two data sets revealed that ketamine increased the power of beta and gamma oscillations in the cortex and thalamus even in the resting state before a stimulus was presented, whereas the amplitude of beta/gamma oscillations after the 200–700 ms stimulus period was significantly lower in all recorded cortical and thalamic sites after ketamine administration.

Ketamine inhibits NMDA receptors involved in the transmission of excitatory signals in the brain. Credit: Izhikevich, Edelman

A post-stimulus time duration of 200–700 ms is long enough to encode, integrate, and perceive the incoming sensory signal. The observed reduction in the strength of oscillations induced by sensory stimuli may be related to impaired perception.

The analysis also revealed that by inhibiting NMDA receptors, ketamine administration added noise to gamma frequencies in the 200–700 ms post-stimulation period in one thalamic nucleus and in one layer of the somatosensory cortex. It can be assumed that this observed increase in noise, i.e. a decrease in the signal-to-noise ratio also indicates an impaired ability of neurons to process incoming sensory signals.

These findings suggest that psychosis may be induced by an increase in background noise disrupting the function of thalamocortical neurons. This in turn may be caused by a malfunction of NMDA receptors affecting the balance of inhibition and excitation in the brain. Noise makes sensory signals less defined or pronounced. In addition, it can cause spontaneous bursts of activity associated with a distorted perception of reality.

“The detected changes in thalamic and cortical electrical activity associated with ketamine-induced sensory information processing disorders may serve as biomarkers for testing antipsychotic drugs or for predicting disease course in patients with psychotic spectrum disorders,” says Sofia Kulikova.

About this neuroscience news

Author: Anastasia Lobanova
source: HSE
Contact: Anastasia Lobanova – HSE
Image: Image attributed to Izhikevich, Edelman

Original Research: Free access.
The psychotomimetic ketamine disrupts the transfer of late sensory information in the corticothalamic network” by Yi Qin et al. European Journal of Neuroscience

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Ketamine has been found to increase brain noise

Summary

The psychotomimetic ketamine disrupts the transfer of late sensory information in the corticothalamic network

In prodromal and early schizophrenia, attentional and perceptual disturbances are associated with structural and chemical brain abnormalities and with dysfunctional corticothalamic networks showing disrupted brain rhythms. The underlying mechanisms are elusive.

The noncompetitive NMDA receptor antagonist ketamine simulates the symptoms of prodromal and early schizophrenia, including disturbances in ongoing and task- and sensory-related broadband beta-/gamma-frequency (17–29 Hz/30–80 Hz) oscillations in corticothalamic networks.

In normal healthy subjects and rodents, complex integrative processes such as sensory perception elicit transient, large-scale synchronized beta/gamma oscillations within a time window of several hundred ms (200–700 ms) after the presentation of the object of attention (eg, sensory stimulation).

Our aim was to use an electrophysiological multisite network approach to investigate, in lightly anesthetized rats, the effects of a single psychotomimetic dose (2.5 mg/kg, s.c.) of ketamine on oscillations evoked by sensory stimuli.

Ketamine transiently increases the strength of baseline beta/gamma oscillations and decreases sensory-induced beta/gamma oscillations. In addition, it disrupted information transfer in both the somatosensory thalamus and the associated cortex and reduced sensory-induced thalamocortical connectivity in the broadband gamma range.

The present findings support the hypothesis that NMDA receptor antagonism disrupts the transfer of perceptual information in the somatosensory cortico-thalamo-cortical system.


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