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The role of the pituitary adenylate cyclase-activating polypeptide (PACAP) in respiration

Presenters Name: 
Alisha Sahu
Co Presenters Name: 
Primary Research Mentor: 
Douglas Bayliss
Secondary Research Mentor: 
Yingtang Shi
9:30 - 10:15
Time of Presentation: 
2019 - 9:30am to 10:15am
Newcomb Hall Ballroom
Presentation Type: 
Presentations Academic Category: 
Grant Program Recipient: 
Harrison Undergraduate Research Grant

Breathing is regulated by a mechanism known as central respiratory chemoreception that responds to changes in the concentration of carbon dioxide in the blood. It has been found that PACAP deficient mice are more prone to sudden postnatal death, perhaps due to reduced chemosensitivity, although the mechanism behind this syndrome is not completely understood (Cummings et al. 2004; Wilson & Cummings, 2008). This study focuses on exploring the role of PACAP in central breathing patterns. In previous experiments, a lentiviral mediated shRNA knockdown was used to specifically knockdown PACAP in the RTN (the breathing control center) of adult experimental mice. A blunted response to the CO2 challenge in the PACAP knockdown mice lead us to believe that the neuropeptide PACAP is an integral part of the breathing network. Additionally, single cell qPCR and histology data show a higher expression of PACAP in neonatal mice. We used Cre/lox recombination techniques to genetically knock out PACAP in Phox2B+ neurons in order to determine whether a burst of PACAP expression at an early age indicates a higher reliance on PACAP for breathing at time of birth. Phox2B is highly expressed in the RTN, so Phox2B Cre mice were crossed with PACAP floxed mice to create a conditional knockout. A preliminary analysis of the data shows a blunted response to the CO2 challenge in the neonatal knockout mice as well as increased time spent in apnea, suggesting a role for PACAP in breathing at time of birth.