Animals learn to distinguish between potentially helpful and harmful stimuli, through the activation of dopamine neurons in the Ventral Tegmental Area, which transiently releases dopamine from terminals in the Nucleus Accumbens and Prefrontal Cortex (PFC). Dopamine release is initiated by the burst-pause firing pattern of dopamine neurons, which is supported in part by potassium channels GIRK (G-protein-coupled inwardly rectifying potassium) and sK (calcium-activated potassium) located on dendrites. These channels are the effectors of important G-protein coupled receptors including GABA, acetylcholine, norepinephrine, and glutamate. During arousal and avoidance or stress behaviors, co-released neuropeptides (i.e. endogenous opioids, endocannabinoids and corticotropin releasing factor, or CRF) regulate neurotransmitter sensitivity. This means that stress can exacerbate drug-seeking behavior. Thus, we use stressful predator odortrimethylthiazoline (TMT) as a means to investigate how these different stress-factors acutely “fine-tune” the dopamine neural sensitivity during natural drug- or reward-seeking behaviors.