Date of Award
Master of Science
Psychological Science (MS)
Adam J. Prus
This study explored the use of optogenetic tools to better understand treatments used for schizophrenia. The “positive” symptoms (e.g., hallucinations, paranoia, etc.) of schizophrenia may come from overexpression of dopamine in mesolimbic dopamine neurons. Positive symptoms can be produced in healthy volunteers treated with amphetamine, a psychostimulant drug and dopamine releaser. Conversely, antipsychotic drugs may reduce positive symptoms by blocking dopamine receptors. This study used optogenetics to explore how drugs that alter neurotransmission, might alter behaviors occurring from activation of mesolimbic dopamine (DA) neurons in the ventral tegmental area (VTA). Light-induced activation of DA neurons in the VTA in male rats produced a significant increase in total distance traveled in an open field and body temperature. Animals treated with amphetamine, a dopamine releaser, also had a significant increase in total distance travelled and body temperature. No significant change was found between trials of amphetamine; it would be logical to think amphetamine depleted neurons of dopamine. However, A D2/3 receptor antagonist did block these effects. These results demonstrate that selective activation of mesolimbic dopamine neurons produces effects similar to amphetamine. Further, they coincide with previous findings that used different research techniques to link amphetamine’s effects to mesolimbic dopamine neurons.
Rice, Remington J., "EFFECTS OF OPTOGENETIC ACTIVATION AND PHARMACOLOGICAL MODULATION OF DOPAMINE NEURONS" (2016). All NMU Master's Theses. 90.