Summary: By inhibiting NMDA receptors, ketamine increases noise at gamma frequencies in one layer of the thalamic nucleus and one layer of the somatosensory cortex. The results suggest that psychosis may be triggered by an increase in background noise impairing thalamocortical neurons, which may be caused by dysfunction of NMDA receptors affecting the balance of inhibition and excitation in the brain.
Source: HSE
An international team of researchers, including Sofya Kulikova, a senior researcher at HSE University in Perm, found that ketamine, being an NMDA receptor inhibitor, increases background noise in the brain, causing higher entropy of incoming sensory signals and disrupting their transmission between the thalamus and the cortex.
This discovery may contribute to a better understanding of the causes of psychosis in schizophrenia.
An article containing the results of the study has been published in the 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 induce 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.
Similar changes in the functioning of NMDA receptors are currently considered to be one of the causes of perceptual disturbances in schizophrenia. However, it is still unclear exactly how this process occurs in the brain regions involved.
To find out, neuroscientists from France, Austria and Russia studied how the brains of lab rats on ketamine process sensory signals. Researchers examined beta and gamma oscillations occurring in response to sensory stimuli in the rodent brain’s thalamo-cortical system, a neural network linking the cerebral cortex to the thalamus responsible for transmitting sensory information from the organs of perception to the brain .
Beta oscillations are brain waves between 15 and 30 Hz, and gamma waves are those between 30 and 80 Hz. These frequencies are considered essential for the encoding and integration of sensory information.
In the experiment, rats were implanted with microelectrodes to record electrical activity in the thalamus and somatosensory cortex, a 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 ketamine administration.
A comparison of the two data sets revealed that ketamine increased the strength of beta and gamma oscillations in the cortex and thalamus even in the resting state before a stimulus was presented, while the amplitude of beta /gamma within 200–700 ms post-stimulation period was significantly lower at all cortical and thalamic sites recorded after ketamine administration.
The 200-700 ms post-stimulation time frame is long enough to encode, integrate and perceive the incoming sensory signal. The observed decrease in the power of oscillations induced by a sensory stimulus may be associated with 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 one layer of the somatosensory cortex. It can be assumed that this observed increase in noise, i.e. a reduction in the signal-to-noise ratio, also indicates the impaired ability of neurons to process incoming sensory signals.
These results suggest that psychosis may be triggered by an increase in background noise impairing the function of thalamo-cortical neurons. This, in turn, could be caused by malfunctioning NMDA receptors affecting the balance of inhibition and excitation in the brain. Noise makes sensory signals less defined or pronounced. Additionally, it can cause spontaneous outbursts of activity associated with a distorted perception of reality.
“Discovered alterations in thalamic and cortical electrical activity associated with ketamine-induced sensory processing disorders could serve as biomarkers for testing antipsychotic drugs or predicting disease course in patients with brain disorders. psychotic spectrum”, explains Sofya Kulikova.
About this neuroscience research news
Author: Anastasia Lobanova
Source: HSE
Contact: Anastasia Lobanova – HSE
Image: Image is credited to Izhikevich, Edelman
Original research: Free access.
“Psychotomimetic ketamine disrupts the transfer of late sensory information in the corticothalamic network” by Yi Qin et al. European Journal of Neuroscience
See also
Abstract
Psychotomimetic ketamine disrupts the transfer of late sensory information in the corticothalamic network
In prodromal and early schizophrenia, disturbances in attention and perception are associated with structural and chemical brain abnormalities and dysfunctional corticothalamic networks with disturbed brain rhythms. The underlying mechanisms are elusive.
The non-competitive NMDA receptor antagonist ketamine mimics the symptoms of prodromal and early schizophrenia, including disturbances of ongoing and related to sensory tasks and senses in the corticothalamic networks.
In normal healthy subjects and rodents, complex integration processes, such as sensory perception, induce large-scale transient synchronized beta/gamma oscillations within a time window of a few hundred ms (200–700 ms) after presentation. of the object of attention (eg sensory stimulation).
Our objective was to use an electrophysiological multisite network approach to study, in lightly anesthetized rats, the effects of a single psychotomimetic dose (2.5 mg/kg, subcutaneous) of ketamine on the oscillations induced by stimuli. sensory.
Ketamine transiently increased the power of baseline beta/gamma oscillations and decreased sense-induced beta/gamma oscillations. Furthermore, it disrupted information transferability in both the somatosensory thalamus and associated cortex and decreased sense-induced thalamocortical connectivity in the broadband gamma range.
The present results support the hypothesis that NMDA receptor antagonism disrupts perceptual information transfer in the cortico-thalamo-cortical somatosensory system.
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