Estrogen receptors (ERs) can be localized to the cell membrane where their activity results in alterations in neurotransmission, neural structure, and behavior. These effects are often mediated by group 1 mGluRs associated with surface ERs. Previous research in our lab has found that 17β-estradiol (17βE) influences spine density in the female rat nucleus accumbens (NAc). In the NAc core (NAcC), 17βE decreases dendritic spine density in an mGluR5 dependent mechanism. In contrast, in the NAc shell (NAcSh), 17βE increases spines via mGluR1. Given that these contrasting effects are a result of 17βE-mediated activation of disparate group 1 mGluRs, we wanted to determine if independent activation of individual group 1 mGluRs would bidirectionally change dendritic spine density in the NAc. Ovariectomized female rats were given a systemic injection of an mGluR5 positive allosteric modulator, CDPPB, at either 5 or 10 mg/kg and sacrificed 24 hours later. Neurons in the NAc were ballistically labeled with DiI, and spine densities were determined. At both doses, CDPPB decreased dendritic spine density throughout the NAc, paralleling the effect of 17βE in the NAcC. Experiments are currently underway to determine if an mGluR1 agonist will increase spine density throughout the NAc, similar to the increase within the NAcSh after 17βE administration. These data would suggest that within the NAc different group 1 mGluRs are functionally coupled to opposing signaling pathways that produce bidirectional effects on dendritic spine density. Furthermore, 17βE has opposing effects on spine density within subregions of the NAc by activating distinct group 1 mGluRs within the NAcC and NAcSh. The ability of 17βE to differentially regulate plasticity within subregions of the NAc may have consequences for the functional output of this brain region.