In cultured astrocytes and microglia from an experimental model of amyotrophic lateral sclerosis (ALS), treatment with the pro-inflammatory cytokines tumor necrosis factor α (TNFα) and interleukin 1β (IL-1β) induced an increase in mGluR3 but a decrease in mGluR5 gene expression [204]; however, in the hSOD-G93A rat ALS model, a robust upregulation of mGluR5 was seen in cultured mutated astrocytes compared to wild-type, though stimulation of the receptor failed to activate astrocytic glutamate uptake [205]. The gene discussed is GRM5; the disease is amyotrophic lateral sclerosis.