The ventral tegmental area (VTA) plays a critical role in motivation and reinforcement. Kappa and mu opioid receptor (KOP-R and MOP-R) agonists microinjected into the VTA produce powerful and largely opposing motivational actions. There are several classes of neuron in the VTA: principal, secondary, and tertiary. Glutamate transmission within the VTA contributes to the motivational effects of opioids. Therefore, information about opioid control of glutamate release onto each class of VTA neuron is important. To address this issue we performed whole cell patch-clamp recordings in VTA slices and measured excitatory postsynaptic currents (EPSCs) in all types of VTA neurons. The KOP-R agonist (trans)-3,4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl)-cyclohexyl] benzeneacetamide methane-sulfonate hydrate (U69593; 1 µM) produced a small reduction in EPSC amplitude in principal neurons (14%), and a significantly larger inhibition in secondary (47%) and tertiary (33%) neurons. The MOP-R agonist [D-Ala², N-Me-Phe⁴, Gly-ol⁵]-Enkephalin (DAMGO; 3 µM) inhibited glutamate release in principal (42%), secondary (45%) and tertiary neurons (35%). Unlike principal and tertiary neurons, in secondary neurons the magnitude of the U69593 EPSC inhibition was positively correlated with that produced by DAMGO. Finally, DAMGO did not occlude the U69593 effect in principal neurons, suggesting that some glutamatergic terminals are independently controlled by KOP and MOP receptor activation. These findings demonstrate that MOP- and KOP-R agonists regulate excitatory input onto each VTA cell type.