Summary: By inhibiting NMDA receptors, ketamine increases gamma frequency noise in one layer of the thalamic nucleus and one layer of the somatosensory cortex. The findings suggest that schizophrenia may be caused by an increase in background noise that disrupts the thalamocortical nerve, which may be caused by a malfunction in the NMDA receptor that affects the balance of inhibition. And excitement in the brain.
Source: ហ. ស
International researchers, including Sofya Kulikova, a senior researcher at HSE-Perm University, have found that ketamine, an NMDA receptor blocker, increases brain noise, which causes an increase in incoming and outgoing emotions. To their transmission between the thalamus and the cortex.
These findings may contribute to a better understanding of the causes of schizophrenia in schizophrenia.
An article with the findings of the study was published in European Journal of Neurology.
Schizophrenic spectrum disorder affects about 1 in 300 people worldwide. The most common manifestations of these disorders are perceptual disturbances such as perception, confusion, and psychosis.
A drug called ketamine can cause a mental state similar to schizophrenia in healthy individuals. Ketamine inhibits NMDA receptors involved in the transmission of excitatory signals in the brain. Imbalances of excitability and inhibition in the central nervous system can affect the accuracy of spiritual perception.
Similar changes in NMDA receptor function are currently believed to be one of the causes of schizophrenia. However, it is still unclear whether this process actually occurs in the area of the brain involved.
To find out, neuroscientists from France, Austria and Russia studied how the brains of laboratory mice react to signals of ketamine processes. The researchers looked at beta and gamma oscillations that occur in response to emotional stimuli in the thalamo-cortical system of the rodent’s brain, a neural network that connects the cerebral cortex with the thalamus responsible. For transmitting emotional information from the organ of perception to the brain.
Beta oscillations are brain waves in the range of 15 to 30 Hz, and gamma waves are in the range of 30 to 80 Hz. These frequencies are believed to be important for encoding and integrating emotional information.
In experiments, mice were implanted with microelectrons to record electrical activity in the thalamus and somatosensory cortex, the areas of the brain responsible for processing emotional information from the thalamus. The researchers stimulated the mice’s whiskey (vibrissae) and recorded brain responses before and after ketamine administration.
Comparison of the two data sets showed that ketamine increased the energy of beta and gamma oscillations in the cortex and thalamus even in the resting state before stimulation was shown, while the amplitude of beta / gamma oscillations in the 200- 700 ms post – Stimulation duration was significantly lower at the cortical and thalamic locations recorded after ketamine administration.
The post-excitation period of 200-700 ms is long enough to encode, input and perceive incoming signals. A observed decrease in the power of emotionally driven oscillations may be associated with impaired perception.
The analysis also showed that by blocking NMDA receptors, ketamine administration added noise to the gamma frequency in the post-stimulation period of 200-7700 ms in a thalamic nucleus and in one layer of the somatosensory cortex. It can be assumed that this increase in noise, i.e., a decrease in the signal-to-noise ratio, also indicates a weakened ability of neurons to process incoming signals.
These findings suggest that schizophrenia may be caused by an increase in background noise that impairs the function of the thalamo-cortical nerve. Conversely, this may be due to abnormal functioning of NMDA receptors that affect the balance of inhibition and excitability in the brain. Noise makes the signal less limiting or pronounced. In addition, this can lead to spontaneous outbursts of activity related to misconceptions of reality.
“Changes found in thalamic and cortical activity associated with disease-related information processing processes caused by ketamine may act as biomarkers for antimicrobial testing or prognosis,” says Sofya Kulikova. Patients with mental spectrum, “says Sofya Kulikova.
About this neuroscience research information.
Author: Anastasia Lobanova
Source: ហ. ស
Contact: Anastasia Lobanova – HSE
Image: This photo was uploaded to Izhikevich, Edelman
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“Psychotomimetic ketamine interferes with slow information transfer in the corticothalamic network” by Yi Qin et al. European Journal of Neurology
Psychotomimetic ketamine interferes with slow information transfer in the corticothalamic network
In prodromal and early-stage schizophrenia, attention and cognitive disorders are associated with structural and chemical abnormalities of the brain and with dysfunctional corticothalamic networks that exhibit brain rhythm. Annoying head. The basic mechanism is difficult to understand.
Non-competitive NMDA receptor antidepressants simulate the symptoms of schizophrenia and early stages, including disturbances in running processes and tasks and awareness regarding beta- / gamma-frequency (17–29 Hz). / 30–80 Hz) oscillations in the corticothalamic network
In normal healthy subjects and rodents, complex integration processes, such as emotional perception, trigger beta / gamma oscillations, which synchronize large scale in the time window a few hundred ms (200-700 ms) after the object display of Attention (e.g., emotional stimulation).
Our goal was to use a multidisciplinary network approach to investigate mice injected with anesthetized effects of a single psychotomimetic dose (2.5 mg / kg, subcutaneous) of ketamine on emotionally driven oscillations.
Ketamine increased transient energy of beta / gamma oscillations and decreased beta / gamma oscillations caused by emotions. In addition, it interferes with the transfer of information in both the somatosensory thalamus and the related cortex and reduces the thalamocortical connections caused by emotions in the gamma broadband range.
The current findings support the hypothesis that NMDA receptor antagonism interferes with the transfer of perceptual information in the cortico-thalamo-cortical somatosensory system.