Skip to content
Licensed Unlicensed Requires Authentication Published by De Gruyter July 1, 2012

Glutamate attenuates nitric oxide release from isolated trigeminal ganglion satellite glial cells

  • J.C. Laursen , R. Somvanshi , U. Kumar , B.E. Cairns , X.-D. Dong , L. Arendt-Nielsen and P. Gazerani



Elevated concentrations of nitric oxide (NO) and glutamate (Glu) in the trigeminal ganglion (TG) may contribute to the development and maintenance of migraine headache. The role of satellite glial cells (SGC) and their pattern of substance release in relation to the pathophysiology of migraine are currently under investigation. In the present study, we investigated the release of NO from isolated trigeminal SGCs and its modulation by Glu.


SGCs from the TG of adult male Sprague-Dawley rats (n = 8) were isolated and maintained in culture until used. SGCs were treated with graded concentrations of Glu (0, 10, 100, 1000 μM) and samples were withdrawn after 48 h of incubation. In subsequent experiments, SGCs were treated with vehicle medium, 10 μM forskolin (FSK) alone, or 10 μM FSK in conjunction with 100 μM Glu and incubated for 48 h. The NO concentration was determined using the Griess Reagent System and data was subjected to a one-way repeated measures ANOVA analysis, where p <0.05 was considered statistically significant. All experimental procedures were performed at minimum in triplicate.


The concentration of NO was 3.59 ± 0.04 M under baseline conditions. Application of 10 or 100 μM Glu resulted in a significant drop in NO concentration (2.92 ± 0.017 μM and 2.83 ± 0.012 M, respectively) compared to baseline, whereas treatment with 1000 μM Glu did not significantly alter NO release. Treatment of SGCs with 10 μM FSK significantly increased NO release (to 125.94 ± 3.90% of baseline) compared to baseline. Coapplication of 10 M FSK with 100 M Glu significantly decreased FSK-induced NO release (83.73 ± 2.29% of baseline), compared to both FSK-mediated NO release and baseline levels.


These findings suggest that one mechanism by which SGCs protect the TG from elevated Glu concentrations that may occur in response to prolonged noxious stimulation is to reduce the release of NO.

Published Online: 2012-07-01
Published in Print: 2012-07-01

© 2012 Scandinavian Association for the Study of Pain

Downloaded on 27.3.2023 from
Scroll Up Arrow