One in 300 people worldwide suffers from schizophrenia-related illnesses. Perceptual abnormalities such as hallucinations, delusions, and psychosis are the most common symptoms of these disorders.
Ketamine can cause psychosis-like mental states in healthy people. Ketamine blocks NMDA receptors, which are involved in the transmission of excitatory signals in the brain. A feeling of imbalance in the excitation and inhibition of the central nervous system can impair the accuracy of perception (
Similar abnormalities in the activity of NMDA receptors are now thought to be one of the causes of the cognitive disorders associated with schizophrenia. However, how this process occurs in brain regions is still unknown.
Neuroscientists from France, Austria and Russia studied how the brains of laboratory rats on ketamine processed sensory input. the transmission of sensory information from the sensory organs to the brain.
Beta oscillations are brain waves that occur between 15 and 30 hertz, while gamma waves occur between 30 and 80 hertz. These frequencies are thought to be important for sensory encoding and integration.
Rats were implanted with microelectrodes to record electrical activity in the thalamus and the somatosensory cortex of the brain, which is responsible for processing sensory information from the thalamus. Before and after ketamine treatment, the researchers stimulated the rats’ whiskers (vibrissae) and recorded brain responses.
Comparison of the two data sets revealed that ketamine increased the power of beta and gamma oscillations in the cortex and thalamus before a stimulus was presented, whereas the amplitude of beta and gamma oscillations was significantly lower at 200–700 ms post-stimulus. at all recorded cortical and thalamic sites after ketamine administration.
A time lag of 200-700 ms after stimulation is sufficient for encoding, integration and comprehension of incoming sensory information. The observed decrease in the power of oscillations caused by a sensitive stimulus can be associated with a decrease in perception. Pre-stimulus beta and gamma frequencies in cortical and thalamic recordings are significantly higher with ketamine than with saline. An analysis published in the European Journal of Neuroscience also found that ketamine administration increased noise to gamma frequencies in a thalamic nucleus and a layer of the somatosensory cortex after activation by blocking NMDA receptors. It is reasonable to assume that the observed increase in noise, i.e. a decrease in the signal-to-noise ratio, is also due to a decrease in the ability of neurons to process incoming sensory information.
These findings suggest that increased background noise may promote psychosis by affecting the activity of thalamocortical neurons. This, in turn, may be caused by NMDA receptor dysfunction, which alters the balance of inhibition and excitation in the brain. Sensory signals are less distinct or pronounced due to noise. In addition, it can result in spontaneous bursts of activity associated with a distorted view of reality.
The lead author of the study, Dr. “The detected changes in thalamic and cortical electrical activity associated with ketamine-related sensory information processing disorders can serve as biomarkers for testing antipsychotic drugs in patients with psychotic spectrum disorders or for predicting the course of the disease,” says Sofya.
- The psychotomimetic ketamine disrupts late sensory information transmission in the corticothalamic network – (https:onlinelibrary.wiley.com/doi/10.1111/ejn.15845)