This discovery might help researchers better understand the origins of psychosis in people with schizophrenia.
An international team of researchers, led by Sofya Kulikova of National Research University Higher School of Economics in Russia, did the studies. According to recently published study, the researchers reported that Ketamine has been discovered to enhance brain noise. Furthermore, it increases the entropy of incoming sensory signals and disrupts their transmission between the thalamus and the cortex. Thus, ketamine can cause the same type of “brain cacophony“/psychosis that individuals with schizophrenia experience.
One in every 300 persons globally suffers from schizophrenic spectrum disease.
Perceptual abnormalities such as hallucinations, delusions, and psychoses are the most prevalent signs of these illnesses. Ketamine, a medication, can cause a mental state akin to psychosis in healthy people.
“The discovered alterations in thalamic and cortical electrical activity associated with ketamine-induced sensory information processing disorders could serve as biomarkers for testing antipsychotic drugs or predicting the course of disease in patients with psychotic spectrum disorders,” says Sofya Kulikova.
The outcome of the study were reported in the European Journal of Neuroscience.
Mechanism behind Ketamine:
Ketamine blocks NMDA receptors which are crucial in the transmission of excitatory impulses in the brain. In the central nervous system, an imbalance between excitation and repression can affect sensory experience.
Neuroscientists from France, Austria, and Russia investigated how the brains of laboratory rats on ketamine interpret sensory inputs. The researchers looked at beta and gamma oscillations in the rat brain’s thalamocortical system, a neural network that connects the cerebral cortex with the thalamus and is responsible for transmitting sensory information from the organs of perception to the brain.
Beta oscillations are brainwaves that occur between 15 and 30 hertz, whereas gamma waves occur between 30 and 80 hertz. These frequencies are thought to be essential for sensory encoding and integration.
Rats were implanted with microelectrodes to record electrical activity in the thalamus and the somatosensory cortex, an area of the brain responsible for processing sensory information from the thalamus. Before and after ketamine treatment, the researchers stimulated the rats’ whiskers (vibrissae) and recorded the brain’s reactions.
Ketamine reveal what causes psychosis:
Ketamine strengthened beta and gamma oscillations in the cortex and thalamus even before a stimulus was applied. This was according to a comparison of the two datasets. In contrast, after ketamine treatment, the amplitude of beta/gamma oscillations in the 200–700 ms post–stimulus interval was significantly reduced at all recorded cortical and thalamic sites.
The observed reduction in the strength of sensory stimulus-induced oscillations can be linked to decreased perception. Ketamine treatment also increased noise in the post-stimulation 200-700 ms interval in one thalamic nucleus and one layer of the somatosensory cortex via blocking NMDA receptors.
This observed increase in noise, i.e. a decrease in the signal-to-noise ratio, may potentially suggest the neurons’ decreased capacity to interpret incoming sensory inputs.
These findings show that an increase in background noise may promote psychosis by affecting the activity of thalamocortical neurons. This, in turn, might be caused by NMDA receptor dysfunction, which alters the balance of inhibition and excitement in the brain. Because of the noise, sensory signals become less distinct or prominent. Furthermore, this may result in spontaneous bursts of activity linked to a skewed view of reality.
Parvathy Sukumaran 
