Ketamine has been found to increase brain noise

An international team of researchers, including HSE University-perm senior researcher Sofya Kulikova, found that ketamine, acting as an NMDA receptor inhibitor, increases background noise in the brain, leading to higher entropy of afferent sensory signals and disrupting their transmission
between the thalamus and cortex.
This finding may contribute to a better understanding of the psychotic causes
of schizophrenia.
An article on the findings has been published in the European Journal of Neuroscience
.

One in every 300 people worldwide has schizophrenia
.
The most common manifestations of these disorders are perceptual disturbances such as hallucinations, delusions, and psychosis
.

A drug called ketamine can induce psychosis-like mental states
in healthy people.
Ketamine inhibits NMDA receptors
involved in excitatory signaling in the brain.
An imbalance of excitation and inhibition in the central nervous system can affect the accuracy of
sensory perception.

Similar changes in NMDA receptor function are currently thought to be one of the
causes of sensory impairment in patients with schizophrenia.
However, it is unclear how this process occurs
in the brain-related regions.

To find out, neuroscientists from France, Austria and Russia studied how the brains of lab rats taking ketamine process sensory signals
.
The researchers examined the β and γ oscillations that occur in response to sensory stimuli in the thalamic-cortical system of the rodent brain, the neural network that connects the cerebral cortex and the thalamus and is responsible for transmitting sensory information from the sensory organs to the brain
.

β oscillations are brain waves in the 15 to 30 hertz range, and gamma waves are brain waves
in the 30 to 80 hertz range.
These frequencies are considered key to
encoding and integrating sensory information.

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

A comparison of the two datasets showed that ketamine increased the intensity of β and γ oscillations in the cortex and thalamus, even at rest before the onset of stimulation, while the amplitude of β/γ oscillations in all recorded cortical and thalamic sites within 200-700 ms after stimulation decreased significantly after ketamine administration
.

A time interval of 200-700 milliseconds after stimulation is sufficient to encode, integrate, and perceive incoming sensory signals
.
The decreased force of oscillations caused by observed sensory stimuli may be related to
impaired perception.

Beta and gamma frequencies recorded by ketamine condition stimulation (right) were significantly higher in the precortex and thalamus compared to normal saline (left).

European Journal of Neuroscience

The analysis also showed that by inhibiting the NMDA receptor, ketamine administration increased gamma-frequency noise
in a thalamic nucleus and a layer of somatosensory cortex during 200-700 ms post-stimulation.
It can be assumed that this observed increase in noise, i.
e.
, a decrease in signal-to-noise ratio, also indicates an impaired
ability of neurons to process afferent sensory signals.

These findings suggest that psychosis may be due to increased background noise impairing the function of
neurons in the thalamic cortex.
This, in turn, may be due to dysfunction of NMDA receptors, affecting the balance
of inhibition and excitation in the brain.
Noise can make sensory signals blurry or inconspicuous
.
In addition, this can lead to spontaneous
bursts of activity associated with distorted perception of reality.

"The discovered changes in electrical activity in the thalamus and cortex associated with ketamine-induced sensory information processing disorders could serve as biomarkers for detecting antipsychotic drugs or predicting the course of illness in patients with psychotic spectrum disorder
.
"