Animal experiment:

For toxicity experiments, mice at PND9 (n=3-9 mice per group) are treated as follows. Two groups receive a subcutaneous (s.c.) injection of corn oil, following, 30 min later, by s.c. injection of either saline or L-Glutamic acid monosodium salt (3 g/kg); two additional groups are treated with 3,4-dihydro-2 H-pyrano[2,3-b]quinolin-7-yl-(cis-4-methoxycyclohexyl)-methanone, dissolving in corn oil (2.5 mg/kg) following, 30 min later, by a s.c. injection of either saline or L-Glutamic acid monosodium salt. In another set of experiments, four groups of crv4 mice or their wild-type littermates (n=5-7 mice per group) are injected s.c. with either saline or L-Glutamic acid monosodium salt (3 g/kg)[1].

L-Glutamic acid monosodium salt (Monosodium glutamate) is an activator of mGlu1 receptor.

A single systemic injection of L-Glutamic acid monosodium salt (MSG) (3 g/kg) to PND9 mice causes extensive retinal degeneration and reduces the number of Brn-3a+RGCs by >70% with respect to control mice treated with saline; In mice treated with L-Glutamic acid monosodium salt and JNJ16259685, the number of RGC is reduced by only<20%, and the resulting value is not significantly different from values obtained in all other groups of mice, including control mice. L-Glutamic acid monosodium salt administration to wild-type BALB/c littermates reduces RGC number to a lower extent than in C57BL/6J mice, but the reduction is still highly significant[1].

[1]. Liberatore F, et al. Permissive role for mglu1 metabotropic glutamate receptors in excitotoxic retinal degeneration. Neuroscience. 2017 Sep 14. pii: S0306-4522(17)30640-1.