Effects of ketamine appear to mirror the neurological changes identified in schizophrenia

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Ketamine increases the level of glutamate in the hippocampus and decreases the connectivity between specific brain areas, according to a study recently published in Molecular Psychiatry.

Recent evidence suggests that a deficit in the function N-methyl-D-aspartate receptor (known as NMDAR) contributes to the glutamate excess that features in schizophrenia. Glutamate is an excitatory neurotransmitter that influences many functions throughout the brain, including learning and memory.

Excessive amounts of glutamate in animals has led to disorganized brain activity. The hippocampus is an area of the brain well known for its role in memory and is particularly susceptible to increases in glutamate. Individuals with schizophrenia often have dysfunctional connections between the hippocampus and frontal and parietal brain regions leading to disorganized neural activity which is thought to be related to deficits in NMDAR.

Small doses of ketamine can block the function of NMDAR in healthy individuals which temporarily produces schizophrenic symptoms. For this reason, ketamine has often been used in research because it produces changes in the brains of healthy people that mimic the brain distortions of people with schizophrenia. However, previous studies have not focused on the effect of ketamine on hippocampal glutamate levels and connectivity in healthy individuals.

In order to investigate the effects of NMDAR blockage on behaviour, a team of scientists from The University of Alabama at Birmingham recruited 15 healthy volunteers to take part in an MRI experiment. Each participant received a small dose of ketamine prior to the scan.

The results showed that ketamine increased the level of hippocampal glutamate and decreased the connectivity between fronto-temporal and temporo-parietal brain regions. These results mirror the neurological changes that have previously been recorded in patients with schizophrenia.

Overall, the results suggest that excess glutamate and abnormal fronto-temporal and temporo-parietal connectivity result from the disruption caused by dysfunctional NMDAR. Additionally, the results of this study support the idea that experimentally inducing diseases such as schizophrenia in healthy volunteers is a viable way to study the associated neurological abnormalities.

The results also suggest that a treatment suppressing glutamate activity in the hippocampus could improve the brain connectivity of patients with schizophrenia and potentially alleviate certain symptoms of the disease.



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