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Pleasure is part of hedonic well-being, with roots back to Epicurus 2000 years ago. With the new evolving neuroscientific methods of the late 20th and beginning of the 21st century, we are now able to study the biological components of pleasure. This thesis aims to review empirical studies on the neural correlates of pleasure, which can have important implications for well-being, and treatment of addiction and affective disorders. Recent studies have suggested that pleasure can be separated into coding and causing. Discoveries show that causing of pleasure is created in so called hedonic hot spots, areas of the brain that intensely creates pleasure in the shell of nucleus accumbens and in the ventral pallidum. Areas that codes pleasure on the other hand is represented into more cortical areas of the brain, including orbitofrontal cortex, anterior cingulate cortex and anterior insular cortex. There has been a growing understanding about how pleasure is represented in the brain, and a discussion on interpretations and limitations are provided followed by future research suggestions in the final section.

Projections from the Nucleus Accumbens (NAc) to the Ventral Pallidum (VP) play a critical role in motivation and reward. Rewards and reward-associated cues are thought to alter this pathway by suppressing GABA release to the VP, however, the role of the NAc to VP pathway has never been investigated with regard to nicotine self-administration. We hypothesized that increasing GABAergic signaling from the NAc to the VP would decrease the reinforcing effects of nicotine. To increase GABA release, CRE dependent DREADD was expressed in the NAc of male rats. Administration of low dose clozapine activated the DREADD receptor and showed a reduction in responding for nicotine suggesting that activation of the NAc to VP pathway reduced reinforcement. However, a nonspecific effect was observed leading to future investigation of locomotor activity. Immunohistochemistry and microdialysis were used to confirm DREADD expression in the NAc and increased extracellular GABA in the VP.