The ventral tegmental area (VTA) is a major site of opioid reward processing. Mu-opioid receptor (MOR) agonism inhibits GABAergic VTA interneurons, thereby disinhibiting dopamine release from nucleus accumbens-projecting VTA neurons. This GABA disinhibition circuit canonically drives opioid-induced reward and opioid-seeking in the VTA. However, we recently discovered MOR-expressing VTA neurons that release glutamate. In opposition to the classic GABA disinhibition model, MOR agonism on glutamatergic VTA neurons decreases activity in VTA dopamine neurons. Here, we investigated the role of GABA-MOR and glutamate-MOR VTA subpopulations in the rewarding, aversive, and somatic consequences of opioid use. Oprm1::Cre mice received VTA infusions of a Cre-dependent vector encoding short hairpin RNA to silence glutamate transmission (via the vesicular glutamate transporter type 2), GABA transmission (via the vesicular GABA transporter), or a control (scrambled RNA sequence). Mice were then tested on fentanyl-conditioned place preference, precipitated withdrawal-conditioned place aversion, fentanyl-induced hyperlocomotion, and precipitated withdrawal symptom quantification. Our preliminary data indicate that silencing GABA transmission from VTA MOR neurons results in reduced fentanyl place preference, increased fentanyl-induced hyperlocomotion, and increased precipitated withdrawal symptoms relative to glutamate silencing and controls.