Many GPCRs can activate dual downstream signaling pathways: one that engages canonical G protein-mediated components, and a second that utilizes β-arrestins as scaffolds and effectors of tyrosine kinase signaling. We are testing the hypothesis that metabotropic glutamate receptors also use β-arrestin-dependent signaling as a largely unrecognized mechanism of altering synaptic strength in cellular models of learning and memory, such as long-term potentiation in the hippocampus. The topical relevance of this research arises from the current academic and industrial efforts to develop mGluR modulators as drugs for a range of neuropsychiatric diseases and the possibility that pharmacological agents biased towards G protein or β-arrestin signaling could produce distinct phenotypic responses and outcomes in patients.