Authors: Calista Greenwood, Ciera Sanders, Pacen Williams, Kaleb Gardner, Caylor Hafen, Hillary Wadsworth
Mentors: Jordan Yorgason
Insitution: Brigham Young University
Dopamine circuit function in the nucleus accumbens (NAc) and ventral tegmental area (VTA) is implicated in the reinforcing effects of drugs of abuse including opioids. Opioid receptor desensitization occurs during acute and prolonged exposure to opioids such as morphine, which may have long lasting effects on dopamine circuit function. Fast scan cyclic voltammetry (FSCV) was performed in mice that have undergone morphine behavioral conditioning. In NAc brain slices, morphine has no apparent direct effects on dopamine release. In contrast, morphine bath application increases VTA dopamine release, which is reversed by naloxone. Interestingly, morphine induced increases in VTA dopamine release were greater in morphine vs saline conditioned mice, supporting a model of circuit sensitization. Surprisingly, blocking voltage gated potassium channels resulted in a switch in morphine effects, where morphine reduced VTA dopamine release. Morphine treated mice had reduced sensitivity to morphine effects on dopamine release in the presence of potassium channel blockers, suggesting that potassium channels are underlying the increases in sensitivity observed in morphine conditioned mice. Experimental protocols were approved by the Brigham Young University Institutional Animal Care and Use Committee according to the National Institutes of Health Guide for the care and use of laboratory animals. Research was funded by Brigham Young University. There are no conflicts of interests to disclose.