Tuberous sclerosis complex (TSC) is a genetic disorder characterized by benign tumors in multiple organs of the body, including the skin, kidneys, liver, eyes, heart, and brain. Neurological impairments are a consistent feature of TSC. These include mental retardation, epilepsy, autism, anxiety, and mood disorders. Currently, there is no cure for TSC and no treatments directed at the cognitive impairments associated with this disorder. The genetic mutation responsible for TSC alters protein synthesis in neurons and disrupts synaptic function. Because regulation of synaptic protein synthesis has been shown to be important for a number of brain functions, including learning and memory, we hypothesize that dysregulation of protein synthesis in TSC may account for the learning and cognitive deficits seen in this disorder. One regulator of synaptic protein synthesis is the metabotropic glutamate receptor. Here, we examine whether metabotropic glutamate receptor function is altered in the mouse model of TSC, and whether pharmacological manipulation of this receptor can restore normal synaptic protein synthesis and function.