Comparative Gene Expression of Leptin in the Amygdala and Dorsal Hippocampus in Response to MDMA Exposure (2024)
Undergraduates: Joe Danica Inigo, Frances Margaret Perez, Emily Clark, Kejia Zhang
Faculty Advisor: Shveta Parekh
Department: Neuroscience
The effects of the synthetic drug 3,4-methylenedioxymethamphetamine (MDMA) have been studied over the years, particularly focusing on its negative physiological and psychological side effects through its action on dopamine, serotonin, and norepinephrine neurotransmitters. While traditionally associated with its recreational use for inducing feelings of well-being, stimulation, and altered sensory perceptions, recent research has focused on its potential therapeutic effects in increasing extroversion and facilitating discussions on emotional topics for anxiety and related disorders. Eating disorders such as anorexia nervosa and bulimia are common anxiety related disorders that affect appetite, yet MDMA’s role as a treatment for these disorders has not been determined. There have been established links between the usage of MDMA and the cocaine and amphetamine regulated transcript (CART), a major player in appetite regulation. CART primarily acts through the regulation of leptin, a hormone that affects appetite. MDMA has also been seen to disrupt memory and learning which is regulated by the dorsal hippocampus and affect fear response which is regulated by the amygdala. However, there is not much research done on the relationship between leptin expression in the amygdala and dorsal hippocampus as a result of MDMA usage. This information can be vital to analyzing MDMA’s role as a therapeutic intervention for eating disorders through the mediation of leptin. We compared adult male rats given an injection of saline as a placebo with those given MDMA 2 hours prior to dissection. Tissue punches of the brain regions of interest were obtained to be then homogenized via RNA extraction and purification. The RNA was quantified prior to RT-PCR, from which the resulting cDNA was run through the qPCR machine as a means to quantify leptin gene expression in rodent brains. The obtained data was statistically analyzed using the comparative CT method through R Studio. We found that MDMA exposure did not significantly affect leptin expression within the amygdala and dorsal hippocampus. These findings suggest that MDMA may not be able to be utilized as a therapeutic intervention for regulating leptin gene expression in these relevant brain regions. However, further research is needed to explore MDMA’s potential impacts on other levels of the leptin pathway or downstream signaling pathways in the same brain regions and/or other brain regions related to appetite regulation. Additionally, future studies could investigate the long-term effects of MDMA on leptin expression, explore MDMA’s effects on other appetite-related hormones, and examine potential sex differences in its effects.