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. Author manuscript; available in PMC: 2012 Feb 1.

Published in final edited form as: Neurochem Int. 2010 Nov 27;58(2):176–179. doi: 10.1016/j.neuint.2010.11.012

(A) C6/mGluR2 cells were treated with SNP (100 μM) to stimulate cGMP formation and IBMX (300 mM) to inhibit phosphodiesterase activity. The group II agonists L-glutamate (100 μM) and LY354740 (10 μM) failed to decrease SNP stimulated cGMP levels. Results are mean ± SEM from four separate transfected cell lines, each assayed in triplicate cultures (n = 12).

(B) cGMP levels in four lines of C6 cells stably transfected with mGluR3 were stimulated with SNP (100μM). NAAG (100 μM) and L-glutamate (100 μM) reduced cGMP levels in these cells. (p>0.05, n = 24 cultures). Overnight incubation with 1 μg/ml of PTX abolished this inhibition.

(A) C6/mGluR2 cells were treated with SNP (100 μM) to stimulate cGMP formation and IBMX (300 mM) to inhibit phosphodiesterase activity. The group II agonists L-glutamate (100 μM) and LY354740 (10 μM) failed to decrease SNP stimulated cGMP levels. Results are mean ± SEM from four separate transfected cell lines, each assayed in triplicate cultures (n = 12).

(B) cGMP levels in four lines of C6 cells stably transfected with mGluR3 were stimulated with SNP (100μM). NAAG (100 μM) and L-glutamate (100 μM) reduced cGMP levels in these cells. (p>0.05, n = 24 cultures). Overnight incubation with 1 μg/ml of PTX abolished this inhibition.