The serotonin system, among other neurotransmitter systems, plays an important role in mood and anxiety disorders. The etiology of mood and anxiety disorders is still largely unknown. The biggest risk factor for the development of mood and anxiety disorders is stress, which has been found to affect neurotransmitter function and behaviors. My dissertation work set out to investigate (1) the effects of in utero stress exposure on neurochemistry and behavior during adulthood and whether concomitant maternal citalopram treatment rescued adverse stress effects, (2) the modulation of serotonin and dopamine by kappa opioid receptors in dysphoria, and (3) the selectivity of optogenetically stimulating dopamine neurons and the interplay between monoamine systems.The project of my graduate work focused on effects of in utero stress exposure and whether treatment with the SSRI, citalopram, could mitigate the adverse effects of prenatal stress. To model anxiety and depressive disorders during pregnancy, I used a mouse model in which pregnant dams underwent a chronic stress paradigm during their pregnancy. A group of dams received concomitant treatment with citalopram, an SSRI. I then examined developmental neurochemistry, and adult neurochemistry and behaviors. Pups from the stressed group had elevated neurochemical and amino acid tissue levels. Moreover, I found that pups born to stressed dams had increases in anxiety- and depressive- like behavior. The stress induced behavioral effects were rescued in pups that received concomitant in utero citalopram exposure. Serotonin concentrations were increased in stress pups after SERT blockade in the vHPC and after a systemic injection of a kappa opioid receptor agonist. My findings suggest beneficial outcomes for treating stress during pregnancy on overall offspring health. The secondary project my graduate work focused on investigating the interplay of serotonin and kappa opioid receptor systems in aversion. Human and animal studies have shown that kappa opioid receptor agonists produce dysphoric mood states. Research has also shown that while KOR agonists have anxiogenic effects, antagonists are anxiolytic. Nonetheless, the mechanisms by which KOR antagonists reduce anxiety-related or dysphoric behavior remain unclear. Using In situ hybridization, I found Oprk1, Sert, vGlut3 and vGat mRNA are co-expressed in the dorsal raphe nucleus, indicating a possible direct or indirect mechanism for KOR-modulation of serotonin transmission. Additionally, I showed local KOR activation with an agonist increases extracellular serotonin levels in both the ventral striatum and ventral hippocampus. This pilot work sets the stage for future studies to concurrently examine neurotransmitter levels during behavioral tests such as conditioned place aversion to better understand the interplay of the serotonin, dopamine, and kappa opioid receptor systems in dysphoria.