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Scientists Discover Ketamine Elevates Brain Activity

By: April Carson



Sofya Kulikova, Senior Research Fellow at the HSE University-Perm, headed up a team of international researchers who found that ketamine - an NMDA receptor inhibitor - amplifies background noise in the brain. This increased level of entropy from incoming sensory signals interrupts their transmission between the thalamus and cortex.


Our breakthrough discovery could bring us one step closer to deciphering the root causes of schizophrenia, as published in the European Journal of Neuroscience. Through further research and exploration into this new understanding, we hope to be able to shed more light on psychosis associated with this mental disorder.


The research team also suggested that ketamine's influence on the brain could lead to new treatments for a variety of psychiatric disorders, including depression, anxiety and bipolar disorder. In addition, our findings open up further avenues of exploration into treating other illnesses such as autism spectrum disorder and addiction.


Worldwide, around one in three hundred individuals have a diagnosed schizophrenic spectrum disorder. These disorders often present with perceptual disturbances including auditory and visual hallucinations, illogical thought processes and potential delusions.


Ketamine, an intriguing medication, has the potential to produce a state of mental confusion in healthy humans. Aspart of its mechanism of action, ketamine suppresses NMDA receptors which are responsible for distributing excitation signals in the brain. An unbalanced ratio between stimulation and inhibition can lead to distortions in sensory perception as well as further cognitive deficits.


In a recent study, scientists have discovered that while ketamine may suppress certain brain processes, it also increases activity in other areas.


Recent research suggests that imbalances in the functioning of NMDA receptors may be a contributing factor to perception disorders observed in schizophrenia. Yet, scientists are still striving to understand exactly how this phenomenon occurs within brain regions implicated with these conditions.


To investigate the effects of ketamine on sensory signals, neuroscientists from France, Austria and Russia performed a study on laboratory rats. They looked into beta and gamma oscillations that arise due to sensory stimuli in the thalamo-cortical system - networks connecting our brain's cerebral cortex with its thalamus which transmit information gathered by our senses.


The scientists administered a dose of ketamine to the rats and observed an immediate elevation in both beta and gamma oscillations. This suggests that it plays a significant role in enhancing sensory information processing, potentially leading to greater awareness of our environment.


Brainwaves between 15 and 30 Hz are called beta oscillations, while those in the range of 30 to 80Hz make up gamma waves. It is believed that these frequencies play a crucial role in processing sensory information and forming memories.


In this groundbreaking experiment, researchers implanted rats with microelectrodes to document electrical activity in the thalamus and somatosensory cortex - an area of the brain accountable for interpreting sensory information from the thalamus. To gauge its impact on neuronal responses, they then triggered stimulation of specific whiskers (vibrissae) prior to and after administering ketamine.


This enabled them to observe alterations in their brains' reactions over time due to ketamine intake.


When comparing the two datasets, ketamine was found to amplify beta and gamma oscillations in both the cortex and thalamus even during rest before any stimulus was presented. Yet when measuring the amplitude of these same oscillations between 200–700 ms after a stimulus had been given, it became evident that they decreased significantly across all recorded cortical and thalamic sites following ketamine administration.


After a sensory signal is experienced, the two hundred to seven-hundred millisecond time period following it can be used to encode, combine and understand it. The observed reduction in power of oscillations caused by stimuli could indicate that perception has been affected.


Our analysis highlighted that blocking NMDA receptors, through the use of ketamine, created more 'noise' in gamma frequencies during the 200-700 ms post stimulation period within one thalamic nucleus and a layer of somatosensory cortex. This increase in noise implies an inability to properly respond to sensory signals. Put simply: neurons are unable to accurately process incoming stimuli following this kind of inhibition.


Our research suggests that psychosis could be activated by an amplified ambient noise, impeding the performance of thalamo-cortical neurons. This may arise from a disrupted functioning of NMDA receptors, leading to disturbances in the brain's balance between inhibition and excitation. The loud noise muddles sensory signals, making it difficult to distinguish between them. This can lead to sudden outbursts of energy as a result of misinterpreted stimuli from the environment.


According to Sofya Kulikova, alterations in thalamic and cortical electrical activity that result from ketamine-induced sensory information processing disorders could serve as markers for testing antipsychotic drugs or predicting how future episodes of psychosis will affect patients with psychotic spectrum disorders.


Structural and chemical brain anomalies, as well as dysfunctional corticothalamic networks displaying disordered brain rhythms, are linked to attentional and perceptual disorders in prodromal and early-onset schizophrenia. Nevertheless, the actual mechanisms contributing to this remain mostly a mystery.


Ketamine, a non-competitive antagonist of NMDA receptors, can produce symptoms similar to those seen in early stages of schizophrenia. This includes disruptions in low and high frequency beta−/gamma oscillations (17–29 Hz/30–80 Hz) within corticothalamic networks during ongoing tasks and sensory processes.


Generally speaking, healthy humans and rodents will display synchronized beta/gamma oscillations on a large-scale within 200 to 700 milliseconds after they are presented with something that has their attention (e.g., sensory stimulation). These processes of integration require only moments to take effect, illustrating the complexity involved.


In a recent study conducted at the University of California, San Diego, researchers have discovered that ketamine has the ability to significantly elevate beta/gamma oscillations in both humans and rodents. The results of this study showed that ketamine induced "rapidly synchronized patterns" of gamma activity throughout several brain regions — a finding with promising implications for understanding brain function.


Ketamine briefly increased the strength of baseline beta/gamma oscillations but decreased sensory-induced beta/gamma frequencies. Furthermore, it inhibited data transfer between both the somatosensory thalamus and related cortex as well as decreasing thalamocortical connectivity within a broad range of gamma waves.


The findings validate the hypothesis that blocking NMDA receptors impairs the delivery of sensory information in this specific pathway.












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April Carson is the daughter of Billy Carson. She received her bachelor's degree in Social Sciences from Jacksonville University, where she was also on the Women's Basketball team. She now has a successful clothing company that specializes in organic baby clothes and other items. Take a look at their most popular fall fashions on bossbabymav.com


To read more of April's blogs, check out her website! She publishes new blogs on a daily basis, including the most helpful mommy advice and baby care tips! Follow on IG @bossbabymav


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