Ketamine Is More Dangerous Than Previously Thought For Healthy People As Shown In New Research
Ketamine, a drug traditionally used as an anesthetic and known for its psychoactive effects, has garnered attention in the medical community for its potential to rapidly treat individuals with mental health conditions who have not responded to traditional antidepressant medications. Despite its history of recreational abuse, the drug shows promise as a novel approach to managing depression and other mental health issues.
There is concern among some psychiatrists about the increasing use of ketamine outside of medical supervision for off-label purposes, as there is not enough evidence to demonstrate the safety of this practice.
To find out more, an international team including Sofya Kulikova, Senior Research Fellow at HSE University-Perm, carried out a study on ketamine use and found that this popular drug may disrupt the transmission of sensory signals between the thalamus and cortex by increasing the brain’s background noise and causing higher entropy of incoming signals.
Schizophrenic spectrum disorders, which affect approximately 1 in 300 people globally, are characterized by hallucinations, delusions, and psychoses, among other perceptual disturbances.
Ketamine, a class of drugs used to treat severe depression, has the potential to cause psychotic symptoms in healthy people. Ketamine blocks NMDA receptors that are crucial in the brain’s excitatory signal transmission. If the central nervous system doesn’t have the right balance of excitation and inhibition, it can change how well the senses work.
Changes in how NMDA receptors work that are similar to these are thought to be one of the causes of perception problems in schizophrenia. But it is still not clear how this process happens in the parts of the brain that are involved.
Neuroscientists from France, Austria, and Russia looked at how the brains of ketamine-treated lab rats interpreted signals from their senses.
In order to understand how sensory stimuli are processed in the brain, the researchers studied beta and gamma oscillations in the thalamo-cortical system of rodent brains. The thalamo-cortical system is a neural network that connects the cerebral cortex with the thalamus and is responsible for transmitting sensory information from the senses to the brain.
Gamma waves are those between 30 and 80 Hz, whereas beta oscillations fall between 15 and 30 Hz. It is thought that these frequencies are essential for encoding and integrating sensory data.
In the experiment, rats were equipped with microelectrodes to record the electrical activity in the thalamus and the somatosensory cortex, a region of the brain that processes sensory information from the thalamus.
Before and after giving the rats ketamine, the researchers stimulated their whiskers (vibrissae) and monitored the brain activity.
According to a comparison of the two sets of data, ketamine appeared to increase the power of beta and gamma oscillations in the cortex and thalamus even in the resting state before a stimulus was presented. However, the amplitude of beta/gamma oscillations in the 200-700 ms period after the stimulus was significantly lower at all recorded cortical and thalamic sites following ketamine administration.
The time gap after stimulation, which ranges from 200 to 700 milliseconds, is sufficient for the encoding, integration, and perception of the incoming sensory data. It’s possible that decreased perception is behind the observed reduction in the strength of sensory stimulus-induced oscillations.
The analysis also showed that ketamine treatment increased noise to gamma frequencies in one thalamic nucleus and in one layer of the somatosensory cortex in the post-stimulation 200-700 ms interval through blocking NMDA receptors.
The increase in noise, or reduction in the signal-to-noise ratio, observed in this study may suggest that neurons have a reduced ability to process incoming sensory signals.
These results imply that an increase in background noise that impairs thalamo-cortical neurons’ ability to operate may be the cause of psychosis. This, in turn, could be brought on by an NMDA receptor failure that upsets the brain’s delicate balance between excitation and inhibition. Sensory signals become fuzzier or less distinct due to the noise. Additionally, this could result in uncontrollable bursts of activity linked to distorted perceptions of reality.
“The discovered alterations in thalamic and cortical electrical activity associated with ketamine-induced sensory information processing disorders,” as explained by Sofya Kulikova, “could serve as biomarkers for testing antipsychotic drugs or predicting the course of disease in patients with psychotic spectrum disorders.”
Image Credit: Julia Rendleman for The Washington Post via Getty Images
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