Dugesia tigrina, commonly known as planaria, have a primitive, yet bilaterally symmetrical centralized nervous system and utilize many of the same neurotransmitters as humans. This allows us to use planaria to study the mechanisms of drug action and the effect of compounds on behavior in a relatively inexpensive in vivo model. Our lab explored the effects of over-the-counter commonly abused drugs on planaria activity, including seizure-like behavior, signs of withdrawal or habituation, or place conditioning. We have found that dextromethorphan (DXM), a cough suppressant contained in most over-the-counter cough medicines, increases seizure-like behaviors and reduces motility in a dose dependent manner.  DXM also has effects on place conditioning and withdrawal. DXM is thought as a non-competitive N-methyl-D-aspartate (NMDA) antagonist, so it can also be compared to the behavioral effects of DXM to that of NMDA stimulation. 

Research on Dugesia tigrina, a species of planaria, has drastically increased over the last decade. Planaria are non-parasitic flatworms that have a primitive, bilaterally symmetrical central nervous system and utilize many of the same neurotransmitters as humans. This makes them a model organism to study drug effects and drug actions on the nervous system. Our lab studies some of the most commonly abused over-the-counter drugs and looks at the behavioral responses of planaria. Our lab has found that Dextrometorphan induces “C” like seizures and screw-like hyperkinesias. I have extended out analysis to look at  Salvia divinorum, an abused drug that can cause hallucinations. Comparing to our previous work with Dextromethorphan, I have found that Salvinorin A, the active component of Salvia divinorum, causes similar and different effects on planaria behavior and motility. This poster reports this comparative analysis. 

Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in the United States and much of the world. NAFLD resembles alcohol-induced liver injury, but occurs in patients with little to no history of alcohol consumption. It is a fairly benign condition, but can progress to a more advanced disease known as nonalcoholic steatohepatitis (NASH); many factors have been implicated in the pathogenesis of this transition (ER stress, mitochondrial dysfunction, insulin resistance, oxidative damage), but the exact mechanism remains unclear. Iron, although essential to many cellular processes, leads to increased oxidative stress and may be significant to NASH development via dysregulation of microRNA expression. To test our hypothesis, we measured microRNAs known to regulate processes marking the transition of NAFLD to NASH, such as apoptosis, inflammation, and lipid metabolism with real-time reverse-transcription PCR in a NAFLD mouse model. By comparing microRNA levels from the liver tissue of iron-treated vs. non-iron-treated NAFLD mice, we can survey effect of iron in exacerbating NAFLD via differential microRNA expression. As a regulator of cellular gene expression by transcriptional inhibition of messenger RNA, microRNA have the capacity to predict cellular processes before physiological changes are seen in the affected tissue. Thus, our results can more specifically describe differentially regulated genes during NASH development in the context of iron. After profiling our treatment groups, we will use bioinformatics to identify gene targets of the significant microRNA and validate the relationship of microRNAs and target genes in vitro. We will also compare the microRNA expression profiles of liver tissue and serum to identify serum biomarkers of NASH. In addition to the mechanistic insights elucidating the pathogenesis of NASH, our findings may lead to alternative non-invasive methods for NASH diagnosis, as liver biopsy is currently the only method for diagnosing NASH.