Until recently, its possible involvement was suggested only by observations of altered expression levels in post-mortem schizophrenia brains [24], [25], where increased mGluR1 expression in the prefrontal cortex has been interpreted as a compensatory change to the NMDA receptor hypofunction [24], as well as by the deficits in sensorimotor gating (prepulse inhibition of acoustic startle) in Grm1 knock-out mice [26] similar to those seen in schizophrenia patients. The gene discussed is GRM1; the disease is schizophrenia.