Adrian Corbett (Committee Member), Sherif Elbasiouny (Committee Member), Christopher Wyatt (Advisor)
Master of Science (MS)
Somatostatin (SST) is a neuropeptide hormone that regulates the release of secondary hormones. Evidence suggests SST plays a neuromodulatory role due to its distribution throughout the central nervous system. Interestingly, SST has been suggested to affect the carotid body, the small peripheral chemoreceptors that regulate breathing. It has been shown that the peripheral chemoreflex sensitivity to CO2 and hypoxia is reduced by SST in humans (Pedersen et al., 1999; Pandit et al., 2014). SST has also been found to inhibit whole cell Ca2+ currents recorded from adult rat carotid body type I cells (e Silva & Lewis, 1995), but the mechanism by which this occurs is unknown. This study aimed to identify the types of SST receptors (SSTR) on type I cells and confirm the mechanism by which their activation inhibits Ca2+ influx. Specific antibodies were used to identify SSTR1-5 on type I cells, and results showed that SSTR1-5 were present on the membrane and cytoplasmically in type I cells. To record intracellular Ca2+ entry, type I cells were loaded with FURA-2 (5 μM) and depolarized in response to stimuli, including 80 mM K+ and hypoxia. Type I cells applied with 2, 10, and 20 minute applications of 1 μM SST had no significant inhibition on voltage-gated Ca2+ entry compared to controls. Also, a 2 minute application of 1 μM SST did not significantly inhibit Ca2+ influx in adult rat type I cells when compared to controls. These results indicate that 1 μM SST does not significantly inhibit K+- nor hypoxic-evoked Ca2+ influx in isolated type I cells from carotid bodies. Thus the mechanism by which SST inhibits the acute ventilatory response to hypoxia and hypercapnia is not likely via inhibition of voltage-gated Ca2+ influx nor via inhibition of the chemosensory response of type I cells.
Department or Program
Department of Neuroscience, Cell Biology & Physiology
Year Degree Awarded
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