Publication Date
2010
Document Type
Thesis
Committee Members
Robert Putnam (Committee Member), Mark Rich (Committee Member), Christopher Wyatt (Advisor)
Degree Name
Master of Science (MS)
Abstract
Type I cells are one of two main cell types located within the carotid body. These cells respond to hypoxia, hypercapnia, and acidosis by releasing excitatory and inhibitory neurotransmitters. This causes increased firing of the carotid sinus nerve and restores blood gas levels to their physiological values. While previous studies have shown whether individual neurotransmitters are excitatory or inhibitory, this work demonstrates how the interplay between two neurotransmitters may potentially shape the output of the carotid body. Histamine, which has previously been shown to have no effect on intracellular Ca2+ in type I cells, may function to modulate the actions of an excitatory neurotransmitter such as acetylcholine. Using Ca2+-imaging techniques, this work shows that histamine inhibits the acetylcholine muscarinic receptor-induced rise in intracellular Ca2+. Histamine, acting on the Gi-coupled H3 receptor, may exert its actions by inhibiting the activation of adenylate cyclase and therefore reducing levels of cAMP. The observed inhibition of muscarinic Ca2+ signaling seems independent of protein kinase A (PKA), as two PKA inhibitors did not mimic the inhibition. Data suggest that Gi-coupled receptor activation may inhibit muscarinic Ca2+ signaling in type I cells by the inhibition of Exchange Proteins Activated by cAMP (Epac).
Page Count
83
Department or Program
Department of Neuroscience, Cell Biology & Physiology
Year Degree Awarded
2010
Copyright
Copyright 2010, all rights reserved. This open access ETD is published by Wright State University and OhioLINK.
