Developmental Variation in Tryptophan Hydroxylase 2 and 5HT1A Receptor Levels in the Bullfrog Brainstem

Bullfrog, Lithobates catesbeiana, is a vertebrate animal model that can be used to study toxicology and developmental physiology. My research aims to examine the brainstem and the pathology of sudden infant death syndrome (SIDS) in humans using a comparative model. Past research demonstrated that caudal raphe neurons send serotonergic fibers that terminate near respiratory neurons in the brainstem. Additional research suggests that late metamorphic tadpoles increase lung burst activity with exposure to low serotonin concentrations mediated by 5-HT1a receptor (5HT1aR) and tryptophan hydroxylase 2 (TH2). I propose that the development of respiratory neurons changes serotonin signaling. Nicotine is a stimulant and paralytic that may interrupt serotonin signaling and impair respiration during larval development. To examine the similarities and differences between humans and bullfrogs, I used the NIH BLAST reference to compare the DNA and amino acid sequences of 5HT1aR and TH2. To determine a baseline, I am performing quantitative western blot analysis of both proteins in adults and tadpoles. Repeating the analysis on nicotine-exposed developing bullfrogs may show shifts during metamorphosis. Impairments to the maturing serotonin network may underlie toxicity in developmental nicotine exposure and further support an increased risk of SIDS. UWL FY23/24 Faculty Research Grant and the UWL 2024 Research Service and Educational Leadership (RSEL) Grant. This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.