Affordable Access

Connecting Inflammation with Glutamate Agonism in Suicidality

Nature Publishing Group
Publication Date
  • Suicide
  • Quinolinic Acid
  • Depression
  • Glutamate
  • Cytokine
  • Medicine And Health Sciences
  • Biology
  • Medicine
  • Pharmacology


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 Asberg 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. Neuropsychopharmacology (2013) 38, 743-752; doi:10.1038/npp.2012.248; published online 9 January 2013

There are no comments yet on this publication. Be the first to share your thoughts.


Seen <100 times

More articles like this

Connecting inflammation with glutamate agonism in...

on Neuropsychopharmacology Mar 12, 2012

The glutamate system as a therapeutic target and i...

on European Archives of Psychiatr... August 2013

Pathways connecting inflammation and cancer

on Current Opinion in Genetics &... Jan 01, 2008
More articles like this..