Researchers have found the probable mechanism whereby the glutamate is a bit more active in the brains of those who make an effort to suicide.These studies have been published online in the journal Neuropsychopharmacology
“The findings are very important simply because show a mechanism of disease in patients,” Brundin, associate professor of translational science and molecular medicine in MSU’s College of Human Medicine, said inside a statement. “There’s been a great deal of center on another neurotransmitter called serotonin approximately 40 years. Concluding from my paper is the fact we should instead turn a few of that focus to glutamate.”
Researchers within this study worked on the spinal fluid of 100 patients in Sweden. They checked the glutamate activity by determining the quinolinic acid which is associated with chemical switch causing glutamate to send more signals to neighboring cells. From the patients, about 67% with the participants were admitted after attempting suicide as the rest were healthy.
Researchers found twofold more quinolinic acid within the cerebrospinal fluid from the suicide attempters in comparison with the healthy people showing elevated glutamate signaling relating to the nerve cells. Moreover, the highest degrees of acid were found in the those that have strongest desire to kill themselves. The patients also showed decreased amounts of quinolinic acid within the patients after few months, in the event the suicidal behavior stopped.
These studies also pointed to the mechanism for inflammation from the brain that might be attributable to quinolinic acid be the immune reaction. Recently, the NMDA-receptor antagonist ketamine has been found for being efficient in removing suicidal behavior.
“In the future, it’s likely that blood samples from suicidal and depressive patients are going to be screened for inflammation,” Brundin said. “It is important that primary medical care physicians and psychiatrists work closely together for this.”
The abstract of this article is as following.
The NMDA-receptor antagonist ketamine has proven efficient in reducing symptoms of suicidality, although the mechanisms explaining this effect have not been detailed in psychiatric patients. Recent evidence points towards a low-grade inflammation in brains of suicide victims. Inflammation leads to production of quinolinic acid (QUIN) and kynurenic acid (KYNA), an agonist and antagonist of the glutamatergic N-methyl-D-aspartate (NMDA) receptor, respectively. We here measured QUIN and KYNA in the cerebrospinal fluid (CSF) of 64 medication-free suicide attempters and 36 controls, using gas chromatography mass spectrometry and high-performance liquid chromatography. We assessed the patients clinically using the Suicide Intent Scale and the Montgomery-Åsberg Depression Rating Scale (MADRS). We found that QUIN, but not KYNA, was significantly elevated in the CSF of suicide attempters (p<0.001). As predicted, the increase in QUIN was associated with higher levels of CSF interleukin-6. Moreover, QUIN levels correlated with the total scores on Suicide Intent Scale. There was a significant decrease of QUIN in patients who came for follow-up lumbar punctures within 6 months after the suicide attempt. In summary, we here present clinical evidence of increased QUIN in the CSF of suicide attempters. An increased QUIN/KYNA quotient speaks in favor of an overall NMDA-receptor stimulation. The correlation between QUIN and the Suicide Intent Scale indicates that changes in glutamatergic neurotransmission could be specifically linked to suicidality. Our findings have important implications for the detection and specific treatment of suicidal patients, and might explain the observed remedial effects of ketamine.
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Reference: Sophie Erhardt, Chai K Lim, Klas R Linderholm, Shorena Janelidze, Daniel Lindqvist, Martin Samuelsson, Kristina Lundberg, Teodor T Postolache, Lil Träskman-Bendz, Gilles J Guillemin, Lena Brundin, (2012). Connecting Inflammation with Glutamate Agonism in Suicidality. Neuropsychopharmacology, doi: 10.1038/npp.2012.248
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