GRM1 and cerebellar ataxia: Mutations that result in excessive mGluR1 signaling have been hypothesized to result in excitotoxicity via a positive-feedback mechanism, in which elevated intracellular calcium potentiates mGluR1-mediated signals.18, 19 Cerebellar Purkinje cells in particular appear acutely sensitive to these fluctuations in calcium levels, which may explain the link between gain of mGluR1 function and the development of cerebellar ataxia.2